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

1. The concentration of catecholamines was measured in several brain areas of the Hewbrew University Sabra rat (SB rat), and in two substrains selected for their respective sensitivity (H) or immunity (N) to hypertension. 2. Hypertension was induced in SB rats by DOCA-salt, renal artery constriction and NaCl 1.7% drinking. The noradrenaline content was consistently elevated in the medulla oblongata of hypertension animals. In other brain areas the rise in noradrenaline varied in the different types of hypertension. 3. Administration of DOCA-salt to H and N rats, while causing marked hypertension in the former, had no effect on noradrenaline in either strain. 4. Untreated, normotensive N rats had in the medulla oblongata, significantly higher concentrations of noradrenaline than did H rats. 5. Differences in brain noradrenaline may explain the inherited susceptibility or resistance to hypertension in H and N rats.
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PMID:Hypertension and brain catecholamine distribution in the Hebrew University Sabra, H and N rats. 28 36

Total exchangeable sodium (Nae) was measured by wholebody counting of 22Na in 1- and 2-kidney Goldblatt rats before, and for 12 weeks after, renal artery clipping. In 1-kidney Goldblatt rats, Nae relative to body weight increased immediately after the clipping procedure and then fell though not to normal levels; from the 10th to the 12th week it again rose rapidly, probably secondary to vascular damage. In 2-kidney Goldblatt rats, Nae relative to body weight increased immediately after the clipping procedure but by the 5th day it was back to normal and remained normal thereafter. Consideration of the values for absolute Nae (i.e. expressed in mmol per rat) casts some doubt on the reality of the sodium 'retention', except in the 1-kidney Goldblatt rats in the later stages of their hypertension. Immediately after surgery temporary loss of weight (presumably mainly affecting fat stores and muscle) probably accounts for much of the rise in Nae relative to body weight.
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PMID:Long-term measurement of total exchangable sodium in one- and two-kidney Golblatt rats. 55

Mexrenoate potassium (SC-26714) is a water soluble salt of a steroidal hydroxy acid which has been shown to antagonize the sodium-retaining effects of aldosterone at oral dosages of 1 mg/kg and about 1.8 mg/kg in the dog and rat, respectively. Dose-related natriuretic responses, indexed as a reversal (increases) in the aldosterone-depressed urinary log Na/K ratio, indicated that mexrenoate was between 2.1 (dog) and 4.5 (rat) times as potent as spironolactone. Based on sodium output, in intact rats, mexrenoate was essentially inactive as a diuretic with an estimated potency of less than 0.4% that of hydrochlorothiazide. Diuretic potency was not indicative of antihypertensive potency. In dogs with established hypertension (Page model with the remaining kidney decapsulated and cellophane wrapped) both mexrenoate and spironolactone exhibited equivalent antihypertensive responses. An optimum oral dose of either compound was 5 mg/kg/day. Initial and maximum antihypertensive responses were observed on the 2nd and 5th days of treatment, respectively. Recovery to pretreatment hypertensive levels was observed 72 hours later. Mexrenoate shares with spironolactone the pharmacological characteristics of an aldosterone antagonist.
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PMID:Mexrenoate potassium: a steroidal aldosterone antagonist and antihypertensive. 86 8

Carvedilol is a multiple-action cardiovascular agent that is both a beta-adrenoceptor antagonist and a vasodilator and has recently been made available for the treatment of mild-to-moderate hypertension. Clinical trials are ongoing to establish the efficacy of carvedilol in angina and congestive heart failure. beta-Adrenoceptor antagonists are known to reduce myocardial work secondary to reductions in heart rate and contractility; accordingly, they have been shown to be cardioprotective in animals and in humans. Because carvedilol has beta-adrenoceptor antagonist activity, it also should provide significant cardioprotection. The additional vasodilating activity of carvedilol, which will further reduce myocardial work by decreasing afterload and myocardial wall tension, should provide more salvage of ischemic myocardium than that afforded by a pure beta-adrenoceptor antagonist, such as propranolol. We investigated the ability of carvedilol and propranolol to reduce infarct size in experimental models of acute myocardial infarction in the rat, pig, and dog. The left anterior descending coronary artery was occluded for 30 (rat) or 45 min (pig) and then reperfused for 24 h (rat) or 4 h (pig). In the dog, the left circumflex coronary artery was occluded for 60 min and reperfused for 24 h. Vehicle, carvedilol, or propranolol was administered intravenously 15 min before ischemia (and, in the rat only, repeated 4 h after ischemia). An additional group of dogs was subjected to permanent left anterior descending coronary artery occlusion for 6 h, and carvedilol or propranolol was given 15 min after occlusion. Infarct size was examined on stained tissue sections using quantitative image analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial protection with carvedilol. 137 42

Idrapril is the prototype of a new chemical class of angiotensin converting enzyme (ACE) inhibitors, the hydroxamic non-amino acid derivatives. Idrapril strongly inhibited rat and human plasma ACE and rabbit lung ACE (IC50: 7-12 nM) as well as the pressor response induced by angiotensin I in anesthetized rats (ED50: 63 nmol/kg i.v.). Idrapril (0.04-23 mumol/kg i.v.) lowered the blood pressure dose dependently, up to 20-35%, in different models of hypertension (sodium-depleted spontaneously hypertensive rat, two-kidney-one-clip renal hypertensive rat, and aortic-coarctated rat), its profile being similar to that of captopril in terms of potency and efficacy. Idrapril and captopril reduced the blood pressure and potentiated substance P-induced bronchoconstriction in the guinea pig to the same extent, suggesting a similar degree of ACE inhibition in the circulation. However, idrapril potentiated capsaicin-induced bronchoconstriction (a model that has been related to the liability of ACE inhibitors to produce cough in patients) less effectively than captopril. We conclude that effective ACE inhibition in vitro and in vivo can be obtained with this novel class of compounds.
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PMID:Pharmacology of idrapril: a new class of angiotensin converting enzyme inhibitors. 138 23

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. With increased dietary sodium chloride intake, the borderline hypertensive rat develops hypertension and exaggerated cardiovascular and renal responses to acute environmental stress, similar to those observed in the hypertensive spontaneously hypertensive rat parent. In other models of sodium chloride-sensitive hypertension with different genetic background (Dahl rat), dietary potassium chloride supplementation protects against the development of hypertension, increased sympathetic nervous system activity, and exaggerated responses to acute environmental stress. This investigation sought to determine whether the dietary sodium chloride-induced development of both the hypertension and the exaggerated responses to acute environmental stress could be reversed or prevented by increased dietary potassium chloride intake. Dietary potassium chloride intake was increased with a 1% potassium chloride drinking solution either after 12 wk of 8% sodium chloride intake (reversal) or concomitant with the onset of 12 wk of 8% sodium chloride intake (prevention). An increase in dietary potassium chloride intake did not reverse or prevent the development of either the hypertension or the exaggerated cardiovascular and renal responses to acute environmental stress in borderline hypertensive rats fed 8% sodium chloride. It is concluded that the difference in genetic background between borderline hypertensive rats and other models of sodium chloride-sensitive hypertension is an important determinant of the protective effect of dietary potassium chloride supplementation.
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PMID:Effect of dietary potassium chloride in borderline hypertensive rats. 139 19

The central role of eicosanoids in reproduction was studied in areas of important clinical interest. First, their involvement in pregnancy-induced hypertension was investigated. Urine of normotensive and hypertensive pregnant women was analysed for 6-keto-PGF1 alpha, TXB2 and PGE2 by HPLC/RIA. PGE2 and 6-keto-PGF1 alpha excretion was markedly reduced in the preeclamptic subgroup of hypertensive patients during the last two trimesters. A reduced urinary excretion of 6-keto-PGF1 alpha, TXB2 and PGE2 was also found in a hypertension animal model (rat). Further, tissue cultures of human placentas, deciduas and fetal membranes from hypertensive pregnancies displayed a reduced prostaglandin production. Secondly, in the same in-vitro model the central role of PGE2 of fetal membrane origin for the beginning or parturition was shown. Thirdly, concerning endometrial function, the enhancement of PGF2 alpha and PGE2 formation in secretory endometrial cells by estradiol-17 beta and progesterone was documented. Fourthly, lipoxygenase product content in peritoneal fluid of endometriotic patients did not differ from controls.
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PMID:The role of eicosanoids in reproduction. 144 35

The role of thromboxane in the gravid normotensive (CD) and hypertensive (SHR) rat was investigated (by utilizing two thromboxane receptor-blocking drugs, EP092 and AH23848) both at mid-gestation and at term. The parameters examined were uterine blood flow (blood flows were measured by the microsphere technique) and uterine weight and placental blood flow at term, fetal mass and number. At mid-gestation EP092 significantly (P < 0.005) increased uterine blood flow in both strains whilst the increases seen with AH23848 were not statistically significant. At term (day 22 in the CD and day 23 in the SHR rat) the antagonists increased uterine blood flow in the CD rats alone. However, at this time the antagonists caused an increase in placental blood flow in both strains. Thromboxane appears to be involved in the regulation of uteroplacental blood flow. The observation that the antagonists were able to potentiate blood flow by mid-gestation may provide a clinical indication with respect to potential prophylactic use of this class of compounds in cases of pregnancy-induced hypertension in women.
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PMID:The role of thromboxane in the uterotrophic response in the gravid normotensive and spontaneously hypertensive rat. 147 32

Angiotensin converting enzyme inhibition markedly suppresses neointima formation in response to balloon catheter-induced vascular injury of the rat carotid artery. To determine whether this effect was mediated through the vasoactive peptide angiotensin II (Ang II), two approaches were followed. First, the balloon model was used to compare the effects of continuous infusion of Ang II, with and without concurrent converting enzyme inhibition by cilazapril; second, the effects of the orally active nonpeptidic Ang II receptor antagonist DuP 753 were analyzed. Morphometric analysis was performed at 14 days after balloon injury. Animals that received continuous infusion of Ang II (0.3 micrograms/min/rat) were found to have significantly greater neointima formation in response to balloon injury than controls. Animals treated with cilazapril (10 mg/kg/day) had markedly reduced neointima formation, but in animals receiving infusion of Ang II, treatment with cilazapril did not suppress development of neointimal lesions. In the second group of experiments, DuP 753 (10 mg/kg twice daily) was as effective to prevent neointima formation as cilazapril. These data support the conclusions that converting enzyme inhibition prevents neointima formation after vascular injury through inhibition of Ang II generation.
Hypertension 1991 Oct
PMID:Role of angiotensin II in injury-induced neointima formation in rats. 183 25

In the kidney, 11 beta-dehydrogenase (11 beta-DH) converts the active steroid cortisol to inactive cortisone (corticosterone to 11-dehydrocorticosterone in the rat). In man, congenital and acquired deficiency of 11 beta-dehydrogenase are rare causes of hypertension in which cortisol acts as a potent mineralocorticoid. Observations from these clinical studies indicate that 11 beta-DH conveys specificity for the mineralocorticoid receptor in distal tubules and collecting ducts. However, while some studies do indicate 11 beta-DH activity in rat distal tubules and collecting ducts, immunohistochemical studies localize 11 beta-DH only to proximal tubules. to resolve this dilemma, we have performed in situ hybridization localization of 11 beta-DH mRNA in rat kidney tissue using 35S-labeled sense and antisense cRNA probes to rat 11 beta-DH. In contrast to our immunohistochemical studies in which 11 beta-DH protein was localized predominantly to proximal tubules in the inner cortex, 11 beta-DH mRNA was expressed in tubules in both the inner and outer cortex, most probably proximal and distal tubules, and in collecting ducts extending across the corticomedullary junction to the papillary tip. Weak hybridization was also seen in glomeruli, but no hybridization to the sense 11 beta-DH cRNA or to sections pretreated with RNase-A was observed. We conclude that renal 11 beta-DH is suitably located to prevent access of glucocorticoid to the MR in an autocrine and not a paracrine fashion. 11 beta-DH in proximal tubules may protect the glucocorticoid receptor.
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PMID:Localization of renal 11 beta-dehydrogenase by in situ hybridization: autocrine not paracrine protector of the mineralocorticoid receptor. 184 10


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