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The luminal diameter of the radial artery was followed by high frequency ultrasound during 50 degrees head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16-45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) omega; P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) 1.min-1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats.min-1], mean arterial pressure (MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]) and total peripheral resistance (TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg.min.1-1 [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa.min.1-1]) increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats.min-1, 46 (SEM 4) mmHg [6.1 (SEM 0.53) kPa] and 18 (SEM 3) mmHg.min.1-1 [2.4 (SEM 0.4) kPa.min-1.1-1], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 +/- 2%) and temporal artery diameters (10 +/- 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.
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PMID:Arterial diameter during central volume depletion in humans. 878 88

The serum concentrations of progesterone and 20 alpha-hydroxypregn-4-en-3-one (20 alpha-OHP) were measured by RIA in blood draining the maternal and fetal sides of the placenta on Day 100 and Day 170 of gestation (term = Day 184) in the baboon to determine the qualitative and quantitative patterns of progestins within the maternal-placental-fetal compartment and to ascertain whether production of placental progestins is increased with advancing gestation. The mean (+/- SEM) concentration of progesterone in maternal serum was similar at mid- (10 +/- 2 ng/ml) and late (11 +/- 3 ng/ml) gestation and not different than that of 20 alpha-OHP (6 +/- 1 ng/ml). In the uterine vein, progesterone levels were greater (p < 0.05) at Day 100 (82 +/- 13 ng/ml) than at Day 170 (30 +/- 7 ng/ml) and exceeded (p < 0.05) those of 20 alpha-OHP at both mid- (8 +/- 2 ng/ml) and late (4 +/- 1 ng/ml) gestation. Progesterone concentrations in the umbilical vein (128 +/- 24 ng/ml) and artery (79 +/- 12 ng/ml) at midgestation exceeded respective values at term (20 +/- 1 and 14 +/- 1 ng/ml). In contrast, 20 alpha-OHP concentrations in the umbilical vein (17 +/- 4 ng/ml) and artery (12 +/- 3 ng/ml) at midgestation increased more than 2-fold by Day 170. The estimated secretion rate of placental progesterone into the fetus was similar at mid- (752 +/- 154 ng/min) and late (681 +/- 171 ng/min) gestation, whereas that for 20 alpha-OHP was negligible at midgestation (57 +/- 71 ng/min) and increased 15-fold (p < 0.05) by term (892 +/- 241 ng/min). Because 20 alpha-OHP is a metabolite of progesterone, total placental progesterone production was greater (p < 0.05) at term (1595 +/- 400 ng/min) than at midgestation (809 +/- 171 ng/min). This study demonstrates that placental secretion of progesterone is bidirectional whereas that of 20 alpha-OHP occurs selectively into the fetus. Although progesterone and 20 alpha-OHP levels in the fetus were lower at term than at midgestation, because of the developmental increase in umbilical blood flow as determined by others, placental progesterone production was actually increased during this interval. Therefore, we suggest that the estrogen-dependent developmental increase in key components of the progesterone biosynthetic pathway, recently demonstrated by us in the baboon placenta, is associated with a corresponding increase in progesterone production.
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PMID:Progesterone and 20 alpha-hydroxypregn-4-en-3-one (20 alpha-OHP) in the pregnant baboon: selective placental secretion of 20 alpha-OHP into the fetal compartment. 887

Three groups of intact hinds (n = 10-18) and one group of ovariectomized hinds were treated with progesterone by mean, of Controlled Internal Drug Releasing (CIDR) devices for 13 days (device removal = Day 0). Group 1 served as controls; group 2 received injections of 4 mg recombinant bovine interferon-alpha,1 twice daily from Days 13 to 21; group 3 was run with a stag from Days 0 to 3, and all hinds were subsequently diagnosed pregnant; group 4 (ovariectomized) was treated with CIDR devices and estradiol to mimic steroid secretion during the estrous cycle. Progesterone profiles were determined from thrice-weekly plasma samples from Days -13 to 28. Rectal temperature was measured in a subset of groups 1 and 2 from Days 9 to 21. Oxytocin-induced prostaglandin F2 alpha release was measured in a subset of groups 1, 2, and 4 on Days 2, 4, 10, 16, and 18. Data are presented as means +/- SEM. Exogenous interferon delayed luteolysis (> or = 28 vs. 21.2 +/- 0.55 days, P < 0.0005) and induced transient pyrexia after the first injection (39.89 +/- 0.11 vs. 38.88 +/- 0.19 degrees C, p < 0.0005). Incidence of oxytocin-induced PGF2 alpha release in control hinds was greater on Days 2 and 18 than on Days 4 and 10 (8/8 and 7/8 vs. 3/8 and 0/8, respectively; p < 0.05) and was greater in control than in interferon-treated hinds on Days 16 and 18 (5/8 and 7/8 vs. 1/8 and 1/8, respectively; p < 0.05). Profiles of plasma progesterone concentration and oxytocin sensitivity in steroid-treated ovariectomized hinds did not differ from those in control hinds. These results suggest that steroid-controlled uterine oxytocin sensitivity is important in luteolysis and is suppressed by the administration of interferon, the putative embryonic pregnancy recognition signal in red deer.
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PMID:Exogenous interferon delays luteal regression in red deer hinds (Cervus elaphus) by suppressing steroid-induced endometrial oxytocin sensitivity. 887 4

1. All previous studies on the effects of changes in sodium intake on the renal dopamine (DA) response (increase in urinary DA output) have used sudden, large changes in oral sodium intake. The present study was designed to study the role of renal DA and the suppression of sympathetic nervous system activity in the natriuretic response to step-wise, gradual increases in sodium intake. 2. Seven healthy, male Chinese subjects (23-25 years) were studied. During the 12-day study period (day -3 to 8), subjects were given the same basic diet containing 1900 calories, 75 g protein, 20 mmol sodium and 45 mmol potassium. From days 1 to 8, subjects also received 'Slow sodium' tablets (Ciba-Geigy) equivalent to 50 mmol on day 1, 100 mmol on day 2, 150 mmol on day 3,200 mmol on day 4, 250 mmol on day 5, and 300 mmol on days 6 to 8. Body weight was recorded and blood pressure was measured after lying supine for 10 min in the morning before breakfast on entry and at the end of the low and high sodium intake periods. Urine was collected for 24 h on day -3 and from days 0 to 8 for the measurement of sodium, potassium, creatinine, free DA and free noradrenaline (NA). 3. After 4 days of sodium restriction, mean arterial pressure (mean +/- SEM) had decreased from 83.0 +/- 1.3 to 79.4 +/- 0.5 (P < 0.05) and body weight from 70.2 +/- 3.1 to 68.3 +/- 3.0 (P < 0.02). Following sodium loading, MAP and body weight did not change, but pulse rate had decreased from 64.1 +/- 2.8 to 57.4 +/- 2.6 (P < 0.02). 4. There was a 13-fold increase in sodium excretion (P < 0.02) by the last day of the high sodium intake period. There were no significant changes in urine volume and urinary excretion of potassium, creatinine and free DA throughout the high sodium intake period. In contrast, there was a 19.9-26.5% decrease in urine NA 4 and 6 days after the start of the increase in sodium intake. 5. Healthy Chinese subjects do not have a renal DA response to gradually increasing sodium intake over an 8-day period. Any tendency to hypervolaemia-related rises in blood pressure during the high sodium intake period may be partly offset by a reduction in sympathetic nervous system activity.
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PMID:Urinary dopamine outputs do not rise in healthy Chinese subjects during gradually increasing oral sodium intake over 8 days. 888 62

CG produced by fetal tissues extends the functional lifespan of the primate corpus luteum during early pregnancy. Previous studies showed that urinary hCG administered to monkeys to simulate the rising CG levels associated with early pregnancy enhanced both progesterone (P) and relaxin (RLX) production by the corpus luteum. The current study was designed: 1) to compare the ability of recombinant (r) and urinary (u) hCG to stimulate luteal function, and 2) to assess the role of P in the regulation of luteal RLX secretion during simulated early pregnancy by concomitant administration of hCG and the 3 beta-hydroxysteroid dehydrogenase inhibitor trilostane to reduce P production. Rhesus monkeys received injections of either r-hCG or u-hCG (Ares Serono) in increasing doses (15-2880 IU/dose, twice daily) for 9 days beginning on day 9 of the luteal phase (n = 5/group). An additional group (n = 4) received r-hCG as described above, with concomitant oral administration of trilostane (500 mg/dose twice daily; Sanofi Winthrop). Daily serum samples were assayed for hCG by immunoradiometric assay, steroid hormones by RIA, and RLX by enzyme-linked immunosorbent assay. Serum hCG levels typically were not different between the r-HCG and u-hCG groups during or after treatment. Concentrations of hCG peaked 1 day after the final injection in monkeys receiving r-hCG (mean +/- SEM. 2759 +/- 120 mIU/mL) and u-hCG (2120 +/- 60 mIU/mL) and dropped below 5 mIU/mL by 10 days after the final treatment in all groups. Both r-hCG and u-hCG stimulated luteal P and RLX production. Progesterone levels rose rapidly after the initiation of hCG treatment and peaked in animals receiving r-hCG (14.4 +/- 2.8 ng/mL) and u-hCG (11.9 +/- 1.4 ng/mL) 4 days after initial administration. RLX levels peaked in the r-hCG (400 +/- pg/mL) and u-hCG (323 +/- 85 pg/mL) groups within 4 days of the final hCG treatment. Trilostane with r-hCG reduced P concentrations to very low levels (< 0.5 ng/mL; P < 0.01) within 1 day of administration compared to those in animals receiving r-hCG only and maintained these low levels for the entire treatment interval. Nevertheless, trilostane administration did not alter luteal RLX production, with serum levels peaking at 377 +/- 76 pg/mL. These data indicate that r-hCG and u-hCG were equally efficacious in stimulating the steroidogenic and peptidergic activities of the corpus luteum during simulated early pregnancy. In addition, P deprivation during r-hCG administration did not alter circulating RLX levels, suggesting that P is not a major regulator of RLX production by the primate corpus luteum during early pregnancy.
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PMID:Stimulation of primate luteal function by recombinant human chorionic gonadotropin and modulation of steroid, but not relaxin, production by an inhibitor of 3 beta-hydroxysteroid dehydrogenase during simulated early pregnancy. 896 69

This study was undertaken to compare the effects of chronic angiotensin-converting enzyme (ACE) inhibition on blood pressure (BP) and renal hemodynamics in older black and nonblack hypertensive patients with chronic renal insufficiency. A multicenter, placebo lead-in double-blind, parallel group study was performed to compare the antihypertensive efficacy and renal hemodynamic response to the once-daily ACE inhibitor fosinopril (n = 14) and lisinopril (n = 13) over a 22-week period. The study goal was to lower diastolic blood pressure (DBP) to 90 mm Hg or less. Furosemide was added after 6 weeks if blood pressure goal was not achieved. At outpatient clinics at university medical centers, 27 older hypertensive patients (> or = 45 years; 12 blacks, 15 nonblacks; 19 male, eight female) with DBP of 95 mm Hg or higher and 4-hour creatinine clearance 20 to 70 mL/min/1.73 m2 were studied. Changes (delta) from baseline in BP, glomerular filtration rate (GFR), and renal plasma flow (RPF) were measured. Mean systolic blood pressure (SBP) and DBP decreased significantly and to a similar extent in randomized groups: fosinopril (mean +/- SEM) delta DBP at 6 weeks was -13 +/- 2 (P < 0.0001; 95% CI, -16 to -9) and at 22 weeks was -12 +/- 2 (P < 0.0001; 95% CI, -16 to -9); lisinopril delta DBP at 6 weeks was -14 +/- 6 (P < 0.0001; 95% CI, -10 to -18) and at 22 weeks was -16 +/- 2 (P < 0.0001; 95% CI, -12 to -21). GFR and RPF did not change significantly in either group. BP was significantly reduced and to a similar extent in blacks and nonblacks: for blacks, delta DBP at 6 weeks was -11 +/- 3 (P < 0.05; 95% CI, -0.01 to -9) and at 22 weeks was -16 +/- 2 (P < 0.0001; 95% CI, -11 to -20); for nonblacks, delta DBP at 6 weeks was -14 +/- 1 (P < 0.0001; 95% CI, -12 to -17) and at 22 weeks was -12 +/- 2 (P < 0.0001; 95% CI, -16 to -8). Eight patients (five blacks and three nonblacks) required an addition of furosemide after 6 weeks to reach the DBP goal of < or = 90 mm Hg at 22 weeks. GFR was not significantly altered for either racial group at 6 weeks; however, at 22 weeks; however, at 22 weeks, GFR decreased significantly in blacks (delta GFR, -16 +/- 5; P < 0.006; 95% CI, -26 to -5) and tended to increase in nonblacks (delta GFR, 7 +/- 6; P > 0.25). delta GFR correlated directly with the delta RPF (delta GFR = 0.0611* delta RPF -2.35 +; r = 0.68; P < 0.003). There was no correlation between delta MAP and delta GFR or delta RPF in blacks or nonblacks. We conclude that chronic ACE inhibition with fosinopril and lisinopril alone or in combination with furosemide lowers BP in older blacks and nonblacks with hypertension and chronic renal insufficiency. Racial differences in the renal hemodynamic response to chronic ACE inhibition were noted and appear to be independent of diuretic use and the magnitude of BP lowering.
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PMID:Racial differences in the renal response to blood pressure lowering during chronic angiotensin-converting enzyme inhibition: a prospective double-blind randomized comparison of fosinopril and lisinopril in older hypertensive patients with chronic renal insufficiency. 918 76

Angiotensin-converting enzyme inhibitors have beneficial effects that are presumably mediated by decreased angiotensin II (ANG II) production. In this study, we measure for the first time ANG I and ANG II levels in the interstitial fluid (ISF) space of the heart. ISF and aortic plasma ANG I and II levels were obtained at baseline, during intravenous infusion of ANG I (5 microM, 0.1 ml/min, 60 min), and during ANG I + the angiotensin-converting enzyme inhibitor captopril (cap) (2.5 mM, 0.1 ml/min, 60 min) in six anesthetized open-chested dogs. ISF samples were obtained using microdialysis probes inserted into the left ventricular myocardium (3-4 probes/dog). ANG I increased mean arterial pressure from 102+/-3 (SEM) to 124+/-3 mmHg (P < 0.01); addition of cap decreased MAP to 95+/-3 mmHg (P < 0.01). ANG I infusion increased aortic plasma ANG I and ANG II (pg/ml) (ANG I = 101+/-129 to 370+/-158 pg/ml, P < 0.01; and ANG II = 22+/-40 to 466+/-49, P < 0.01); addition of cap further increased ANG I (1,790+/-158, P < 0.01) and decreased ANG II (33+/-49, P < 0.01). ISF ANG I and ANG II levels (pg/ml) were > 100-fold higher than plasma levels, and did not change from baseline (8,122+/-528 and 6,333+/-677), during ANG I (8,269+/-502 and 6, 139+/-695) or ANG I + cap (8,753+/-502 and 5,884+/-695). The finding of very high ANG I and ANG II levels in the ISF vs. intravascular space that are not affected by IV ANG I or cap suggests that ANG II production and/or degradation in the heart is compartmentalized and mediated by different enzymatic mechanisms in the interstitial and intravascular spaces.
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PMID:Compartmentalization of angiotensin II generation in the dog heart. Evidence for independent mechanisms in intravascular and interstitial spaces. 921

This study was conducted to determine if reducing sympathetic tone with alpha 1-adrenergic receptor blockade affected the maximal forearm vascular conductance (FVCmax, reactive hyperemia) responses in young borderline hypertensives and normotensive controls. The FVC response following ischemia (14 min arterial occlusion with 3 min of hand exercise) was determined after systemic alpha 1-blockade (5 mg prazosin in preceding 24 h) in hypertensives (n = 11, MAP = 110 +/- 1, age = 24.5 +/- 1.1, mean +/- SEM) and normotensives (n = 13, MAP = 82 +/- 1, age = 22.5 +/- 0.3). During the placebo trial, resting FVC was lower in the hypertensives than the normotensives (.0472 +/- .0073 vs .0755 +/- .0095 units; P < .05). During alpha 1-blockade, FVC did not differ between the groups. Within each group, FVCmax did not differ significantly between either trial. During placebo, FVCmax was lower (P < .05) in the hypertensives (.3485 +/- .0335 vs .5641 +/- .0503 units) and remained so during alpha 1-blockade (.4048 +/- .0520 vs .5286 +/- .0275 units; P < .05). These data suggest that alpha 1-blockade does not increase FVCmax in borderline hypertensives and that both functional and structural changes in the peripheral vasculature are involved in the blood pressure elevations seen in this group.
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PMID:Effects of alpha 1-blockade on maximal vascular conductance in young borderline hypertensives. 938 72

The knowledge about the structure and function of the protein families responsible for cGMP synthesis and metabolic conversion has grown vastly the last years, whereas little is known about proteins that account for the cellular export of cGMP. In the present study, we have employed a model with inside-out vesicles prepared from human erythrocytes to characterize modulation and regulation of cellular cGMP extrusion. The active transport was saturable (Km of 2.4 +/- 0.2 microM, mean +/- SEM, n = 3) and coupled to ATP hydrolysis since no accumulation was detected in the presence of ATP-gamma-S and AMP-PNP. The observation that 100 microM of cAMP caused a minimal inhibition (14.4 +/- 0.3%) of active cGMP transport showed that the extrusion system for cGMP was not shared with cAMP, but a competitive interaction occurred for the ATP-independent association to the inside out vesicles. In contrast, the lowest, but physiological relevant cAMP concentrations (0.1-5 microM) stimulated the active cGMP transport with 30-35%, an observation that suggests cAMP as an allosteric regulator of the cGMP transporter. Several well-known modulators of other energy-requiring membrane transport systems caused a competitive and concentration-dependent inhibition, including verapamil (Ki = 13.0 +/- 2.4 microM), forskolin (Ki = 13.5 +/- 1.4 microM) and probenecid (Ki = 27.0 +/- 1.3 microM). Progesterone, which was the most potent inhibitor (Ki = 2.2 +/- 0.3 microM), interacted with the active cGMP transport in a noncompetitive manner. The highest concentration (100 microM) of IBMX and theophylline reduced the active cGMP uptake with 29.5 +/- 1.9% and 21.6 +/- 2.1%, respectively. None of these substances interfered with the association of cGMP to the vesicles in absence of ATP. The present results show that human erythrocytes possess a cell membrane cGMP transporter which is coupled to an ATPase. Its activity is regulated by cAMP in an apparent allosteric manner and inhibited by substances previously known to interact with other membrane transport systems.
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PMID:Cyclic AMP stimulates the cyclic GMP egression pump in human erythrocytes: effects of probenecid, verapamil, progesterone, theophylline, IBMX, forskolin, and cyclic AMP on cyclic GMP uptake and association to inside-out vesicles. 945 9

In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9+/-3.5 (mean+/-SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K+) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K+ was supplemented to 170 mmol/d (KHCO3). On the last day of each study week, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) using renal clearances of PAH and inulin. Ten subjects were salt sensitive (SS) (DeltaMAP >+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m2) decreased from 920+/-75 to 828+/-46 (P<0.05); filtration fraction (FF, %) increased from 19. 4+/- to 21.4 (P<0.001); and renal vascular resistance (RVR) (10(3)xmm Hg/[mL/min]) increased from 101+/-8 to 131+/-10 (P<0.001). In all subjects combined, DeltaMAP varied inversely with DeltaRBF (r =-0.57, P=0.02) and directly with DeltaRVR (r = 0.65, P=0.006) and DeltaFF (r = 0.59, P=0.03), but not with MAP before NaCl loading. When supplemental KHCO3 abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K+-deficient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity.
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PMID:NaCl-induced renal vasoconstriction in salt-sensitive African Americans: antipressor and hemodynamic effects of potassium bicarbonate. 1002 19

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