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

The purpose of these experiments was to compare the contractile response to ACh of stomach fundal strips from hypertensive (SHR) and normotensive (WKY) rats during the development of hypertension. The results indicate that the reactivity to ACh is the same in fundal strips from young SHR and WKY rats; however, with maturation strips from WKY rats undergo a reduction in responsiveness which does not occur in the SHR. Therefore, strips from older SHR rats are more reactive to ACh than are those from age matched WKY rats.
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PMID:Changes with hypertension and maturation in the response of stomach fundus to acetylcholine. 674 93

The density of [3H]quinuclidin-3-yl benzilate ([3H]QNB) binding sites in the posterior hypothalamus was determined in spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats at the ages of 1, 3, 11 and 50 weeks. In SHR, even at the early age of 1 week which is prehypertensive, the values obtained were 1.5 times greater than those of age-matched WKY rats. The values of the equilibrium dissociation constant (KD) did not differ between SHR and WKY rats of the same age. In the pons medulla, however, the density of [3H]QNB binding sites was not different between the two strains of rats of matching age. Isolation-induced hypertension in adult Wistar rats and an increase in the density of [3H]QNB binding sites in the posterior hypothalamus were observed to arise concomitantly. A hypothesis is offered whereby a relative increase in ACh receptor sites in the posterior hypothalamus is a primary cause of hypertension in the models considered.
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PMID:The muscarinic cholinergic receptors in the posterior hypothalamus of hypertensive and normotensive rats. 716 Apr 35

We investigated the influence of aging and hypertension on the vasorelaxant effect of calcitonin gene-related peptide (CGRP), examining the responses to stimulation of perivascular vasodilatory nerves and to administration of the peptide in isolated mesenteric vascular bed preparations of young (aged 2-3 months) and old (aged 18 months) normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). We used preparations preconstricted by perfusion with 100 microM methoxamine with addition of 5 microM guanethidine. The stimulation-induced vasorelaxation in the preparations of young SHR animals was significantly lower than that in those of age-matched WKY rats. Moreover, the vasodilator response to stimulation displayed an age-dependent decline in vascular beds of normotensive animals. The degree of the relaxant response to CGRP (0.01-1 microM) did not differ significantly between vascular preparations of normotensive and hypertensive rats; but was significantly reduced in preparations of both SHR and WKY rats aged 18 months as compared with those of young animals. An age-dependent decrement in the vascular reactivity, qualitatively similar to that observed with CGRP, was also detected with two other vasodilators, i.e., the endothelium-dependent vasodilator acetylcholine (ACh 0.1-100 microM) and the directly acting nitrovasodilator sodium nitroprusside (SNP, 1-10 microM). We conclude that the vascular sensitivity to CGRP, as well as that to other vasodilator agents acting by different mechanisms, decreases with age in both normotensive and genetically hypertensive rats.
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PMID:Effects of aging and hypertension on vasorelaxant activity of calcitonin gene-related peptide: a comparison with other vasodilator agents. 751 87

We examined whether the altered rostral ventrolateral medulla (RVLM) cholinergic function in spontaneously hypertensive rats (SHR) results from enhanced presynaptic cholinergic tone. Male 12- to 16-week-old SHR and age-matched Wistar Kyoto rats (WKY) were anesthetized, paralyzed and artificially ventilated. Unilateral microinjection of cholinergic agents into the RVLM produced a pressor response. The pressor response to physostigmine was greater in SHR than that of WKY whereas the response to ACh and carbachol was the same in WKY and SHR. Bilateral microinjection of scopolamine produced a decrease in blood pressure. The depressor response was greater in SHR than that of WKY. When a microdialysis probe was placed in the RVLM, ACh release in the RVLM was greater in SHR than that of WKY. Choline acetyltransferase (CAT) activity was increased only in the rostro-ventral part of the medulla, which contained the RVLM, but not in other parts of the medulla oblongata. Physostigmine (0.5 mg/kg, i.p.)-induced increases in ACh content were also enhanced only in the rostro-ventral part of the medulla. These results provide direct evidence that ACh release in the RVLM is enhanced in SHR. It appears that the enhanced cholinergic activity in the RVLM of SHR results from an increase in cholinergic impulse flow in the RVLM of SHR. This abnormality may play a role in the maintenance of hypertension in SHR.
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PMID:Enhanced release of acetylcholine in the rostral ventrolateral medulla of spontaneously hypertensive rats. 758 59

The hypothesis was tested that plasma from ischemic hindlimbs facilitates hypertension. Ischemia-induced hypertension was generated in rats by infrarenal aortic cross clamping for 5 h after which plasma was obtained from femoral vein blood. In vitro contractile activity of naive aortic rings incubated for 2 h in plasma collected from ischemic rats demonstrated reduced relaxation to acetylcholine and nitroglycerin. Methylene blue (10(-5) M) induced greater contraction in rings incubated in control vs. ischemic plasma, suggesting that endogenous guanylate cyclase activity is decreased by ischemic plasma. However, 8-bromo-guanosine 3',5'-cyclic monophosphate (cGMP) relaxed equally strips incubated in ischemic or control plasma. Acetylcholine-induced nitrite release was significantly lower in ischemic vs. control plasma-incubated strips (8.6 +/- 2.7 vs. 28.2 +/- 2.3 ng/10 mg tissue wt, respectively). The impaired relaxation to acetylcholine in ischemic plasma-incubated rings was significantly increased by L-arginine but not by prior treatment of ischemic plasma with heating or superoxide dismutase and catalase. These findings suggest the impaired relaxation is mediated through inhibition of the nitric oxide-cGMP pathway. Prolonged blunting of vasodilation by ischemic plasma may therefore contribute to maintenance of a sustained vasoconstriction and ischemic hypertension.
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PMID:Inhibition of vascular nitric oxide-cGMP pathway by plasma from ischemic hindlimb of rats. 763 55

Although it is well established that nitric oxide contributes to the regulation of resistance arterial tone in humans, its role at the level of large arteries is less clear. Therefore, we assessed in healthy volunteers the effect of local administration of the inhibitor of nitric oxide synthesis NG-monomethyl-L-arginine (L-NMMA) on basal radial artery diameter (transcutaneous A-mode echotracking) and radial blood flow (Doppler) as well as on the radial response to acetylcholine and the nitric oxide donor sodium nitroprusside. A catheter was inserted into the brachial artery for measurement of arterial pressure and infusion of L-NMMA (2, 4 and 8 mumol/min for 5 minutes, n = 11), acetylcholine (3, 30, 300 and 900 nmol/min for 3 minutes, n = 8), and nitroprusside (2.5, 5, 10, and 20 nmol/min for 3 minutes, n = 6). None of the treatments affected arterial blood pressure or heart rate. L-NMMA dose-dependently decreased radial blood flow (from 31 +/- 6 to 17 +/- 3 10(-3) L/min after 8 mumol/min, P < .01) but did not affect radial artery diameter (from 2.93 +/- 0.11 to 2.90 +/- 0.14 mm). Acetylcholine dose-dependently increased radial blood flow (154 +/- 43% after 900 nmol/min) and radial artery diameter (16 +/- 4%), and both effects were markedly reduced after L-NMMA (increase in radial blood flow and radial artery diameter: 22 +/- 20% and 3 +/- 2%, respectively; both P < .01 versus controls). Nitroprusside also dose-dependently increased radial artery diameter (14 +/- 4% after 20 nmol/min) but only moderately affected radial blood flow (47 +/- 21%).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Aug
PMID:Role of basal and stimulated release of nitric oxide in the regulation of radial artery caliber in humans. 763 43

We investigated endothelium-dependent responses of thoracic aorta isolated from age-matched male and female spontaneously hypertensive rats (SHR) to explore gender differences in endothelial dysfunction that may contribute to the sexual dimorphism observed in the development of hypertension in this strain. Endothelium-dependent relaxation in response to acetylcholine (10(-9) to 10(-4) mol/L) was significantly greater in female rats than in male rats, although impaired responses were seen in both sexes compared with normotensive controls. Inhibition of cyclooxygenase by indomethacin (10(-5) mol/L) improved endothelium-dependent relaxation, but it did not abolish the gender difference. Relaxations in response to sodium nitroprusside were identical in denuded aortic rings from male and female SHR. Acetylcholine at higher concentrations (10(-6) to 10(-4) mol/L) induced endothelium-dependent contraction in intact, quiescent aortic rings from male SHR but not in those from female SHR. After incubation with NG-nitro-L-arginine (10(-4) mol/L), contraction in response to acetylcholine became apparent in rings from female SHR, but it was still significantly less pronounced than in similarly treated rings from male SHR. Endothelium-dependent contraction was prevented by indomethacin in both sexes, suggesting that a cyclooxygenase product such as endoperoxide may be mediating this effect. Because responses evoked by the thromboxane/endoperoxide receptor agonist U46619 (10(-10) to 10(-6) mol/L) were not greater in rings from male SHR than those from female SHR, increased smooth muscle responsiveness or higher thromboxane/endoperoxide receptor density in the males could not account for the differences in endothelium-dependent contraction. These results suggest that sex steroid hormones may control endothelium-dependent vascular reactivity.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Apr
PMID:Gender difference in endothelial dysfunction in the aorta of spontaneously hypertensive rats. 772 92

Renovascular hypertension alters endothelial-dependent mechanisms to affect the response of small arterioles in skeletal muscle to sepsis. Small arteriole responses to sepsis differ between skeletal muscle and small intestine in normotensives. Our study now shows that renovascular (1K1C) hypertension alters small arteriole responses in the small intestine to Escherichia coli sepsis. Large arterioles (A1, A2) constricted by 10-20% in the small intestine of both normotensive and hypertensive rats during both high and low cardiac output sepsis. Small arterioles (premucosal A3 and preserosal A4) constricted during high cardiac output sepsis in normotensive but not hypertensive rats. Small A3 and A4 arterioles dilated (20-40%) during low cardiac output sepsis in hypertensives; but only A3 and not A4 arterioles dilated in normotensives during low cardiac output sepsis. Acetylcholine, which releases endothelial-derived relaxing factor in skeletal muscle, dilated both premucosal A3 and preserosal A4 in both normotensive and hypertensive rats. Thus, hypertension alters small arteriole responses to sepsis in both skeletal muscle and small intestine, but apparently by different mechanisms.
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PMID:Altered microvascular responses of the small intestine to sepsis during renovascular hypertension. 774 28

Pulmonary vascular reactivity was assessed during diagnostic heart catheterization in two patients with pulmonary hypertension unexplained by pulmonary or cardiac disease and in five patients with atypical chest pain and normal coronary arteriograms. Acetylcholine, an endothelium-dependent vasodilator that also has a direct contracting effect on vascular smooth muscle cells, was infused in the right atrium in a step-wise increasing dose in order to obtain final blood concentrations in the pulmonary circulation ranging from 10(-6) mol/L to 10(-4) mol/L. In the five control patients, acetylcholine induced a dose-related decrease of pulmonary vascular resistance (-52 percent +/- 9 percent). In the patients with primary pulmonary arterial hypertension, however, acetylcholine caused a paradoxic increase of pulmonary arterial pressure and of pulmonary vascular resistance. Thus, it appears that endothelium-dependent vasodilation is impaired in the pulmonary circulation of patients with primary pulmonary arterial hypertension. Endothelial dysfunction in the pulmonary circulation may play a role in the pathophysiology of this disease.
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PMID:Paradoxic pulmonary vasoconstriction in response to acetylcholine in patients with primary pulmonary hypertension. 777 7

The role of EDRF in the modulation of blood pressure and vascular reactivity in estrogen-treated rats was investigated both in vivo and in vitro studies. In vivo, long-term subcutaneous injection of ethinyl estradiol (EE2, 0.2 micrograms/day, s.c.) for 6 weeks significantly induced an elevation of systolic blood pressure from 117.1 +/- 2.7 to 129.9 +/- 3.6 mmHg. In vitro, the endothelium-dependent relaxation of ACh (10(-8)-10(-5) M) in intact aortic rings from EE2-treated rats was significantly blunted compared with normal control rats. Meanwhile, the contractile responses to PE (10(-8)-10(-5) M) was no difference between intact and denuded aortic rings from EE2-treated rats. The results indicate that the reduction of vasodilator response to ACh and the loss of enhanced contractile responses to PE in denuded rings may be due to altered endothelial function after long-term treatment with EE2. Furthermore, the high potassium (12.5-62.5 mM) induced-contraction and nitroglycerin (3 x 10(-8)-3 x 10(-6) M) induced-relaxation were not different between EE2 and control groups. These results indicate that the function of vascular smooth muscle did not alter after long-term treatment with EE2. In conclusion, the alteration of function of endothelium may play an important role in the modulation of estrogen-induced mild hypertension.
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PMID:The role of EDRF in the modulation of blood pressure and vascular reactivity in estrogen-treated rats. 795 10


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