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

The present investigation contractile responses of microdissected intrarenal arcuate arteries from sham-operated rabbits and two-kidney, one clip Goldblatt hypertensive rabbits at 2 and 12 weeks after procedure. Arcuate arteries from both kidneys of the sham-operated rabbits and stenotic and nonstenotic kidneys of the Goldblatt hypertensive rabbits were studied. Mean arterial blood pressures of the sham-operated and Goldblatt hypertensive rabbits were 72 +/- 2 and 85 +/- 2, and 130 +/- 3 and 125 +/- 4 mm Hg at 2 weeks and 12 weeks, respectively. In vitro isometric contractile force measurements were made with a small-artery myograph. Responses to graded concentrations of norepinephrine were evoked in the arcuate arteries, and the maximum active force was developed and -log EC50 was determined. At 2 weeks after procedure, the maximum responses of the vessels from the left kidney of the sham-operated rabbits and those from the stenotic left kidney of the Goldblatt hypertensive rabbits did not differ. The responses of the vessels from the right kidney of the sham-operated rabbits did not differ from those of the nonstenotic right kidney of the hypertensive rabbits. A markedly depressed maximum response of the vessels from the nonstenotic kidney of the hypertensive as compared with the right kidney of the sham-operated rabbits was found at 12 weeks after procedure, whereas the vessels from the stenotic kidney of the hypertensive and the left kidney of the sham-operated rabbits exhibited almost identical maximal responses. Responses to U 46619 were similarly affected in the two groups of rabbits. Cold-induced contractile responses of the arcuate arteries from the nonstenotic kidney of the hypertensive rabbits did not differ from those of the sham-operated rabbits at the 12-week interval.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Jun
PMID:Contractility of intrarenal arteries in Goldblatt hypertensive rabbits. 216 93

This study was undertaken to verify the activity of plasma kininases in hypertension. Male Wistar rats (WIS) were used and three models of experimental hypertension were studied: spontaneously hypertensive rats (SHR), renal hypertensive rats, made according to the method of Goldblatt, DOCA-salt hypertensive rats. Normal Wistar rats, nephrectomized rats and sodium-loaded rats were used as control groups. Plasma from these animals was used to evaluate the kininase activities: kininase II activity (KII) was measured by the hydrolysis of hippuryl-L-histidyl-L-leucine (HHL); kininase I activity (KI) was measured by the hydrolysis of hippuryl-L-arginine (HLA) (CN1 activity) and of hippuryl-L-lysine (HLL) (CN2 activity). The three enzyme activities were characterized by their kinetic constants and the inhibitory pattern of various inhibitors. In normal WIS rats, hydrolysis of HHL proceeds with a Km of 2.55 +/- 0.22 mM and at a Vmax of 0.357 +/- 0.017 mumol/min/ml; the enzyme is inhibited by EDTA, 0-phenanthroline and captopril. HLA has a Km of 6.93 +/- 0.32 mM and a Vmax of 0.748 +/- 0.019 mumol/min/ml while the Km and Vmax values of HLL are 35.8 +/- 1.52 mM and 13.11 +/- 0.40 mumol/min/ml. The hydrolysis of both substrates is inhibited by EDTA, 0-phenanthroline and MERGETPA. KII activity is decreased in WKY and SHR rats (Vmax = 0.241 +/- 0.014 and 0.262 +/- 0.011 mumol/min/ml, respectively). In renal hypertensive rats and DOCA-salt hypertensive rats, the KII activity remained unchanged. CN1 activity was increased in 1K, 1C hypertensive animals (Vmax = 0.866 +/- 0.221 mumol/min/ml) and in DOCA-salt hypertensive rats (Vmax = 1.119 +/- 0.049 mumol/min/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Activity of plasma kininase I and kininase II in hypertensive rats]. 217 85

Atrial natriuretic peptide (ANP) is secreted by the heart in response mainly to atrial distension and circulates in plasma in picomolar concentrations. It binds to receptors in blood vessels which it relaxes, renal glomeruli where it induces increased glomerular filtration rate, renal papilla to produce natriuresis, adrenal glomerulosa cells to inhibit aldosterone secretion, and median eminence and pituitary where it may inhibit vasopressin secretion. In experimental models of hypertension plasma levels of ANP are uniformly elevated, except in spontaneously hypertensive rats, in which plasma ANP may only rise transiently. The action of ANP on smooth muscle cells of the blood vessel wall results in production of cyclic GMP, which appears to be the second messenger producing relaxation of pre-contracted blood vessels. Mechanisms other than cGMP generation have been proposed but remain unproven as mediators of ANP action. Receptors for ANP in blood vessels are of two subtypes: B-receptors (or R1-receptors), which contain guanylate cyclase in their structure, and C-receptors (or R2-receptors), which have not been shown to the present to be biologically active. Our studies on vascular ANP receptors are reviewed. In several experimental models of hypertension such as saralasin-insensitive 2-kidney, 1-clip and 1-kidney, 1-clip Goldblatt hypertensive rats and in DOCA-salt hypertensive rats, we have found elevated plasma ANP, as well as decreased binding and ANP-induced vascular relaxation and blood pressure-lowering effects of ANP. Both the B and C ANP receptors appear decreased in density, even after acid washing of membranes to remove any retained circulating ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vascular receptors for atrial natriuretic peptide in hypertension. 217 36

Urinary digoxin-like factor, ADH, sodium and potassium excretion and urine osmolality were studied during the development of two pathogenically different models of hypertension, DOCA-salt (low-renin) and Gold-blatt 2 kidney-1 clip (renin-dependent). Urinary digoxin-like factor was increased in rats that were given saline (NaCl 1%) to drink, uninephrectomized-salt and DOCA-salt rats, with no significant differences between the two groups urinary ADH was elevated in DOCA-salt rats during the study, compared with uninephrectomized-salt rats. Urinary digoxin-like factor and urinary ADH were not significantly modified in Goldblatt 2 kidney-1 clip and sham-operated rats. In addition, positive correlations between digoxin-like factor urinary excretion and urinary ADH and also with sodium urinary excretion were found. These data suggest that: a) digoxin-like factor and ADH could play a role in the pathogenesis of DOCA-salt but not in Goldblatt 2 kidney-1 clip hypertension. b) A common mechanism may stimulate ADH and digoxin-like factor simultaneously. c) Digoxin-like factor plays a role in the control of urinary sodium excretion.
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PMID:Urinary excretion of digoxin-like factor (DLF) and ADH during DOCA-salt and Goldblatt 2 kidney-1 clip hypertension development. 219 65

Recent reports indicate that cyclooxygenase inhibitors such as aspirin may facilitate the release of interleukin-2 from thymic T cells. We have previously reported that aspirin has antihypertensive effects in the standard animal model of essential hypertension, the spontaneously hypertensive rat (SHR). Because the SHR has been reported to be deficient in T cells, it was of interest to determine whether the course of hypertension in this model could be altered by interleukin-2, the T cell growth factor. A single bolus of interleukin-2 (5,000 units/kg s.c.) prevented the increase of blood pressure in the young SHR and lowered pressure to normotensive levels in the well-established hypertensive adult SHR. In the latter, the effects of a single dose have been found to persist for at least 6 months with no toxic or untoward effects apparent. Blood pressure in Goldblatt, single-kidney wistar-kyoto rats, a model of renal hypertension, was not affected by interleukin-2.
Hypertension 1990 Jan
PMID:Antihypertensive effect of interleukin-2. 213 45

Removal of the arterial clip (unclipping) in one-kidney, one-clip (1K, 1C) Goldblatt hypertensive rats causes rapid return of mean arterial pressure (MAP) to normotensive levels. An extracorporeal circulation was established between the renal and jugular veins to evaluate the influence of unclipping on renal blood flow (RBF) in Inactin-anesthetized 1K, 1C rats. MAP in rats with the extracorporeal circulation was 182 +/- 5 mmHg before unclipping or sham operation. MAP decreased to 113 +/- 4 mmHg within 2 h after unclipping compared with 169 +/- 13 mmHg in sham-unclipped rats. RBF increased by 2.8 ml.min-1.g-1 from a basal level of 3.8 +/- 0.3 after unclipping and was maintained approximately 40% above the basal level for 2 h, although renal vascular resistance was 94% greater than in uninephrectomized control rats. Heart rate did not change in either unclipped or sham-operated rats. Indomethacin (7 mg/kg) did not affect unclipping-induced changes in MAP, RBF, or urine output; however heart rate decreased immediately after unclipping and remained approximately 25-35 beats/min below control levels for the 2-h observation period. In rats lacking the extracorporeal circuit, MAP decreased (P less than 0.005) and heart rate increased (P less than 0.05) in response to unclipping. Nevertheless, unclipping-induced tachycardia was significantly less than that caused by nitroprusside infusions causing similar decrements in MAP. The results suggest that the sustained increment in RBF after unclipping in chronic, established 1K, 1C hypertension may be associated with postunclipping hypotension and diuresis, that blockade of prostaglandin synthesis may unmask unclipping-induced bradycardia, and that prostaglandins are not essential for postunclipping changes in renal hemodynamics.
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PMID:Postunclipping renal blood flow in one-kidney, one-clip hypertensive rats. 230 5

A reduction in the density of small arterioles (rarefaction) has been reported in several vascular beds of the spontaneously hypertensive rat (SHR). There have been conflicting reports on the existence of rarefaction in the pial vasculature of SHR. In this study, we determined whether there was rarefaction of pial arterioles in several models of hypertension. We studied SHR; two-kidney, one-clip Goldblatt hypertensive rats; deoxycorticosterone-salt hypertensive rats; and Dahl salt-sensitive rats fed high salt diet. The two groups of normotensive controls were Wistar--Kyoto rats and Dahl salt-sensitive rats fed low salt diet. The duration of hypertension was about 2 months. Density of first-, second-, third-, and fourth-order arterioles was determined by counting the number of vessels from enlarge photographs. We also measured the lengths of segments of the arterioles. We did not observe any evidence of rarefaction of arterioles in the pial vasculature in any of the hypertensive groups of rats. We conclude that (i) rarefaction of arterioles does not occur in the pial microvasculature after approximately 2 months of hypertension and (ii) rarefaction of pial arterioles does not account for abnormalities in the cerebral circulation of hypertensive rats such as protection of the blood-brain barrier or changes in autoregulation of cerebral blood flow.
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PMID:No rarefaction of cerebral arterioles in hypertensive rats. 232 49

We reported that the pups of one kidney:one-clip Goldblatt hypertensive (HT) rats have a predisposition to the induction of experimental hypertension. To investigate the nature of the predisposition, pups of HT dams were challenged with vasopressor agents at 28-days-of-age or treated with DOCA and 6.5% salt diet between 35 and 81 days-of-age. Pups of HT dams had a significantly greater blood pressure between 28 and 81 days-of-age and also showed a greater change in blood pressure when provided a 6.5% salt diet than did pups of normotensive dams. Pups of HT dams demonstrated a decreased bradycardic response after injection of angiotensin II (p less than .05) and a lesser change in mean arterial blood pressure after injection of angiotensin II or norepinephrine than did the pups from normotensive dams. These results suggest an effect of maternal hypertension on the development of cardiovascular control mechanisms in her offspring. The decreased pressor response suggests the predisposition is not due to an increased vascular sensitivity to vasopressors.
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PMID:Cardiovascular correlates of predisposition to hypertension in pups of one kidney: one clip renal hypertensive dams. 234 96

The reduction in blood pressure to normotensive levels within 3 hours of unclipping the one-kidney, one clip Goldblatt hypertensive rat has been attributed to the release of potent blood pressure-lowering lipids, one of which is thought to be identical to platelet activating factor. The specific platelet activating factor receptor antagonist WEB 2086 was infused intravenously into hypertensive one-kidney, one clip rats, and the mean arterial blood pressure changes after unclipping were examined. Before infusion, blocking doses of WEB 2086 were confirmed to effectively abolish the fall in blood pressure induced by exogenous platelet activating factor. Serotonin release in response to exogenous platelet activating factor was also inhibited in platelets preincubated with plasma from rats infused with the antagonist. Hypertensive rats were given a bolus blocking dose of WEB 2086 (5 mg/kg i.v.) and the same dose by infusion (5 mg/kg/hr i.v.) before they were unclipped. A control group was given a bolus volume of saline and infused with saline before unclipping. In WEB 2086-treated rats, blood pressure fell from a baseline mean of 181 +/- 13.0 to 125 +/- 23 mm Hg after 4 hours, a fall of 28%. Saline-treated rats fell from a mean of 194 +/- 23 to 127 +/- 25 mm Hg (33%). There was no significant difference in the blood pressure fall between the two groups. Therefore, platelet activating factor is unlikely to be responsible for the restoration of normal blood pressure after unclipping the Goldblatt hypertensive rat. We attribute the fall in blood pressure to other presently unidentified renomedullary lipids.
Hypertension 1990 Jun
PMID:Platelet activating factor and one-kidney, one clip hypertension. 234 25

The present study was performed to determine the role of afferent arterioles in the impaired autoregulatory response shown to occur in the contralateral kidney of Goldblatt hypertensive rats. The responsiveness of juxtamedullary afferent arterioles to alterations in perfusion pressure was studied in the nonclipped kidney of two-kidney, one clip hypertensive and sham-operated rats. Systolic pressure, 5-6 weeks after clipping, averaged 184 +/- 6 mm Hg in the hypertensive rats (n = 16) and 121 +/- 3 mm Hg in the sham-operated control rats (n = 7). By using the in vitro blood-perfused juxtamedullary nephron technique, afferent arterioles were directly visualized, and their inside diameters were measured by videomicroscopic methods. In sham-operated kidneys perfused with blood from normotensive rats, afferent arteriolar diameter averaged 22.8 +/- 1.8 microns at a renal arterial perfusion pressure of 151 +/- 1 mm Hg and increased to 24.8 +/- 1.8 microns when perfusion pressure was reduced to 110 +/- 2 mm Hg. Conversely, in hypertensive kidneys perfused with blood from either hypertensive or normotensive rats, the afferent arterioles failed to vasodilate and actually exhibited a slight decrease in diameter from 24.6 +/- 1.3 to 23.0 +/- 2.3 microns in response to the same reduction in perfusion pressure. Vasodilator capability, however, could be demonstrated in response to verapamil and sodium nitroprusside, which increased afferent diameter in both the sham-operated and hypertensive groups of rats. Thus, unlike arterioles from normotensive rats, juxtamedullary afferent arterioles from two-kidney, one clip Goldblatt hypertensive rats fail to vasodilate after a reduction in perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Jun
PMID:Afferent arteriolar responsiveness to altered perfusion pressure in renal hypertension. 235 27


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