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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The arterial and central venous concentrations of angiotensin I (AI), Val5-angiotensin II ([Val5]AII), and Val5-angiotensin III ([Val5]AIII(2-8)) were quantitatively determined in conscious sheep before and after sodium depletion. All three angiotensins were elevated in blood with progressive sodium loss. During sodium deficiency the arteriovenous concentration ratios (A:V) of AI, [Val5]AII, and [Val5]AIII(2-8) were found to be 0.48 +/- 0.03 (n = 9), 1.30 +/- 0.05 (n = 16), and 1.52 +/- 0.05 (n = 11) respectively. Intravenous infusion of [Val5]AII or [Val5]AIII(2-8) significantly elevated the A:V of respective angiotensins, being 2.09 +/- 0.28 (n = 5) for [Val5]AII and 2.2 +/- 0.37 (n = 6) for [Val5]AIII(2-8). The blood clearance rates of exogenous [Val5]AII and [Val5]AIII(2-8) in sodium-depleted sheep were calculated to be 135 +/- 15 liter/hr (n = 10) and 140 +/- 13 liter/hr (n = 10) respectively. Based on these experimental data, a steady-state model of angiotensin metabolism was constructed. If it is assumed that endogenous arterial blood [Val5]AII and [Val5]AIII(2-8) cleared metabolically at a similar rate as exogenous arterial blood angiotensins, it can be calculated that at steady-state 55% of the arterial [Val5]AII concentration was derived from the peripheral vascular bed. For [Val5]AIII(2-8), 63% of the arterial concentration was derived from the pulmonary circulation. The concentration of [Val5]AIII(2-8) in arterial blood was 42% of [Val5]AII.
Hypertension
PMID:Angiotensin I, II, and III in sheep. A model of angiotensin production and metabolism. 702 9

Angiotensin tachyphylaxis is rapidly induced in the mesenteric vascular circuit of the rat perfused with a saline solution. there is crossed tachyphylaxis among angiotensins (AI, AII, and AIII). The angiotensin antagonist Sar 1-Ileu 8-AII is ineffective when the vascular preparation is previously rendered tachyphylactic to AII, showing that the AII receptors are not available during tachyphylaxis. This finding supports the theory that angiotensin tachyphylaxis is caused by receptor occupancy by the agonist. By perfusing the vascular preparation with aII solutions that were too diluted to produce vasoconstriction, tachyphylaxis to AII was induced. Therefore, AII receptors can be slowly saturated without producing vasoconstriction. The recoveries of the vasoconstrictor effect of AII and AIII at 30 and 60 minutes after tachyphylaxis are similar; thus, the dissociation constants of the AII- and AIII-receptor complexes should be alike. After three bolus injections of AI, the vascular preparation is completely refractory to AI, AII, and AIII. When the conversion of AI to AII is inhibited with captopril, AI no longer induces tachyphylaxis to AII and AIII. Thus, tachyphylaxis to AII and AIII induced by AI seems to be due not to the occupancy of AII receptors by AI but to the AII formation from AI "in situ."
Hypertension
PMID:Angiotensin I, II, and II tachyphylaxis in the mesenteric vascular circuit of the rat. 702 14

The effects of a single dose of 50 mg of SQ 14225 (Captopril) and 0.6 microgram/kg/min infusion of angiotensin II antagonist, [Sar1, Ileu8] (AII-A), were examined in six patients with dialysis resistant hypertension and seven with normal blood pressures. A depressor effect of Captopril was observed even in patients with AII-A unresponsive dialysis resistant hypertension. The fall in mean arterial pressure (MAP) was significantly correlated with the fall in the total peripheral resistance index (TPRI) following both Captopril administration (r = 0.883, P less than 0.01) and AII-A infusion (r = 0.735, P less than 0.01). Basal plasma renin activity (PRA) was the same in patients with dialysis resistant hypertension as in normotensive patients and correlated with the fall in MAP induced by AII-A infusion (r = -0.640, P less than 0.05). It was concluded that the direct effect of the renin-angiotensin system was uncertain in patients with dialysis resistant hypertension and that the depressor effect of Captopril was not secondary to the suppression of angiotensin II formation.
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PMID:Comparison of the immediate hemodynamic effects of SQ 14225 (Captopril) and [Sar1, Ileu8] angiotensin II in patients with dialysis resistant hypertension. 703 97

Rats were exposed continuously to Pb in utero and after birth by giving their mothers, during pregnancy and lactation, drinking water containing 0, 100, or 500 ppm Pb (as Pb acetate) and then continuing this regimen after weaning. Male rats received 100 ppm developed a significant elevation of systolic blood pressure (152 +/- 3.7 mm Hg vs. 135 +/- 5.6 for controls) at 3 1/2 months and remained hypertensive until sacrifice at 6 months; 500 ppm rats remained normotensive. Both 100 ppm and 500 ppm females remained normotensive. At 6 months, PRA was significantly reduced in the 100 ppm male group but was normal in the 500 ppm group. There were dose-dependent decreases in the AII/PRA ration and in renal renin. Pulmonary converting enzyme activity was not changed by Pb exposure. Blood [Pb] was 40 and 71 mug/dl, respectively, and kidney [Pb] was 4.8 and 22.9 mug/gm. Renal histology was normal in the 100 ppm group. We conclude that doses of Pb which produce blood [Pb] seen in many people are capable of inducing modest hypertension in male rats; higher doses fail to do so. The hypertension is associated with a reduction in PRA and All and therefore is unlikely to be due to hyperactivity of the RAS. (J Lab Clin Med 99:354, 1982.)
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PMID:Lead, hypertension, and the renin-angiotensin system in rats. 705 62

The effect of naloxone upon water consumption by rats was assessed using two intensities each of IV NaCl (Hyperosmolarity), SC polyethylene glycol (hypovolemia), and IV angiotensin II. In each case naloxone produced a dose-related reduction in the amount drunk. Angiotensin-induced drinking was most easily inhibited, and was abolished by only 1 mg/kg naloxone. In contrast, 1 mg/kg naloxone produced only a 50% reduction NaCl-induced drinking, and hypovolemia-induced drinking was not completely reversed by 5 mg/kg. Naloxone was without effect upon the natriuresis after NaCl, or the hypertension during AII administrations. Parallels are drawn between the effects of naloxone on these types of thirst, and of other perturbations including brain damage and taste adulteration.
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PMID:Comparison of the suppression by naloxone of water intake induced in rats by hyperosmolarity, hypovolemia, and angiotensin. 705 17

Approximately one half of the aldosterone-producing adenomas (APA) removed from patients with primary aldosteronism in the Hypertension Unit at Greenslopes Hospital belong to a subgroup in which aldosterone levels are responsive to the renin-angiotensin system (angiotensin-responsive APA; AII-R-APA), unlike classical APAs in which aldosterone is unresponsive (AII-U-APA). Renin mRNA levels in AII-R-APA were elevated when compared with those in AII-U-APA or normal adrenal cortices. Renin mRNA levels in some adrenal cortices surrounding AII-R-APA (but never in AII-U-APA) were raised, suggesting that a genetic defect is not confined to the tumor. Renin gene RFLP analysis in peripheral blood DNA revealed a significant difference in allelic frequencies between patients with AII-R-APA and AII-U-APA, suggesting an association between an alteration in the renin gene and aldosterone responsiveness to the renin-angiotensin system in patients with APAs.
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PMID:The renin gene and aldosterone-producing adenomas. 770 15

1. Normokalaemic primary aldosteronism (PA) masquerades as 'essential hypertension', and 50% of patients with aldosterone-producing adenoma (APA) are normokalaemic at presentation to this unit. 2. Angiotensin-responsive (AII-R) APA is as common as angiotensin-unresponsive (AII-U) APA, and requires adrenal venous sampling for differentiation from bilateral adrenal hyperplasia (BAH). 3. From 1981 to 1992, 55 patients with APA underwent unilateral adrenalectomy and were followed up for at least 12 months postoperatively. Hypertension was cured in 55% and improved in the remainder. 4. Cure rate was lower (P < 0.001) in males (11/32, 34%) vs females (19/23, 83%), lower (P < 0.005) in patients over 45 years of age (13/33, 39%) vs those 45 years or younger (17/22, 77%), lower (P < 0.05) in AII-R APA (11/28, 39%) vs AII-U APA (19/27, 70%) and tended to be lower (not significant) in normokalaemic APA (7/17, 41%) vs hypokalaemic APA (23/38, 61%). 5. A higher proportion (P <0.001) of AII-R APA patients were males (23/28, 82%) vs AII-U APA (9/27, 33%), and a higher proportion were from the older age group AII-U APA 13/27, 48%; P < 0.05). Females with AII-U APA who were hypokalaemic had a very high cure rate (16/17, 94%). 6. Since unilateral adrenalectomy cures or improves blood pressure in normokalaemic and AII-R as well as in hypokalaemic and AII-U patients, all hypertensives should be screened for PA, and AII-R APA differentiated from BAH in proven PA.
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PMID:Response to unilateral adrenalectomy for aldosterone-producing adenoma: effect of potassium levels and angiotensin responsiveness. 792 99

During a double-blind, randomized study in hypertensive patients, changes in plasma lipid and lipoprotein levels during treatment with celiprolol were compared with those occurring during nifedipine treatment. Fifty-three patients (28 men and 25 women) with mild-to-moderate hypertension, aged 20-64 years, were studied. After a 1-month placebo run-in period, patients were randomly assigned to receive either nifedipine (40 mg daily) or celiprolol (200 mg daily), each time using a double-dummy technique. After 6 weeks, dosages of each drug could be doubled. After 6 weeks, there were no differences in plasma lipids between the two treatment groups. However, the changes after 12 weeks of treatment were different (p < 0.05) between the groups, leading to lower levels of plasma esterified cholesterol, low-density lipoprotein (LDL) cholesterol, and apoprotein AI, AII, and B in the celiprolol group. Plasma lecithin cholesterol acyltransferase activity (LCAT) was not modified. The present study showed that celiprolol was at least equivalent to nifedipine in terms of secondary effects on plasma lipids and lipoprotein.
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PMID:Effects of celiprolol vs. nifedipine on serum lipoproteins in patients with mild to moderate hypertension. 794 68

The central effect of angiotensin II on cardiovascular activity has been investigated in conscious trout bearing an intracerebroventricular (i.c.v.) cannula and an intra-arterial catheter. I.c.v. injection of the angiotensin II agonist [Asn1,Val5]AII (6.2-50 pmol) induced a dose-dependent increase in heart rate and arterial blood pressure. Central administration of the angiotensin II antagonist DuP 753 (5 nmol) 30 min before i.c.v. injection of [Asn1,Val5]AII totally prevented the tachycardia and reduced the hypertension induced by the angiotensin II agonist. Intra-arterial injection of arginine-vasotocin (12.5 pmol) caused a bradycardia associated with a marked increase in arterial blood pressure. I.c.v. injection of [Asn1,Val5]AII totally blocked the bradycardia induced by arginine-vasotocin and this effect was prevented by central administration of DuP 753. In contrast, [Asn1,Val5]AII did not affect the increase in blood pressure induced by arginine vasotocin. Suppression of the vagal tone by atropine treatment totally blocked the central effect of [Asn1,Val5]AII. These results show that angiotensin II acts directly on the trout brain to increase blood pressure and heart rate. The effect of angiotensin II is mediated through a receptor related to the mammalian AT1 receptor type.
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PMID:Intracerebroventricular administration of angiotensin II increases heart rate in the conscious trout. 798 71

In this study, we examined the relation between serum lipid levels, gender, and cardiovascular and neuroendocrine stress reactivity in patients with mild hypertension. Ninety-nine individuals (62 men, 37 women) with mild hypertension performed four mental stress tasks: mental arithmetic, public speaking, cold stress, and a computer videogame. Cardiovascular reactivity scores were computed by subtracting the minimum resting blood pressure (BP) and heart rate (HR) values from the maximum values obtained during each task. Neuroendocrine reactivity was calculated as the change from epinephrine and norepinephrine values from mean rest to mean task. High and low reactors were identified on the basis of median splits of reactivity scores, averaged across all four stressors. High systolic blood pressure reactors had higher levels of total (TC), low-density lipoprotein cholesterol (LDL-C), and apo-B than did low reactors. High diastolic blood pressure reactors had lower levels of high-density lipoprotein cholesterol (HDL-C) and higher levels of LDL-C and apo-B than did low reactors. High HR reactors had higher apo-AI:apo-AII ratios than low reactors. Lipid levels were not different for high and low epinephrine and norepinephrine reactors. Although women were noted to have more favorable lipid profiles than men, both male and female hypertensive patients who were high reactors had less favorable lipid profiles than low reactors.
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PMID:Serum lipids, neuroendocrine, and cardiovascular responses to stress in men and women with mild hypertension. 803 18


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