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

Serum angiotensin converting enzyme (ACE) activity and plasma renin activity (PRA) were studied during the development of the widespread necrotic arterial disease that occurs in the induction phase of one-kidney perinephritis hypertension. Control serum ACE activity was significantly higher in rabbits developing many arterial lesions than it was in rabbits developing relatively few arterial lesions. Serum ACE decreased 7 days after the production of unilateral perinephritis in all rabbits. Following contralateral nephrectomy, serum ACE decreased further in rabbits devloping many arterial lesions but returned toward control values in rabbits developing relatively few arterial lesions. Significant inverse correlations were demonstrated for the total number of arterial lesions that developed relative to a) the decrease in serum ACE activity 7 days after the production of unilateral perinephritis, b) the lowest or the average serum ACE activity during the period of development of the arterial lesions after contralateral nephrectomy, and c) the change in serum ACE activity during the period of development of the arterial lesions. Chronic treatment with SQ 20,881, a synthetic nonapeptide inhibitor of ACE activity, during the period of development of the hypertension and the arterial lesions significantly reduced the serum ACE activity and the hypertension but did not change interrelationships between serum ACE activity and the number of arterial lesions that developed. PRA significantly decreased after the production of perinephritis and decreased somewhat further during the induction period of the hypertension after contralateral nephrectomy. No relationships were demonstrated between PRA, or changes in PRA, and the development of arterial lesions. The increase in blood pressure during the incubation period of the hypertension did not correlate with the number of arterial lesions that developed. These finding indicate that serum ACE activity reflects importantly on the capacity to develop necrotic arterial lesions during the induction phase of one-kidney perinephritis hypertention and on functional events relating to their pathogenesis.
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PMID:Serum angiotensin converting enzyme activity and the capacity to develop hypertention-associated arterial disease. Studies during the induction phase of one-kidney perinephritis hypertension in rabbits. 21 77

Cerebral and ocular microaneurysms were produced in rabbits made hypertensive by surgically induced silk-turpentine perinephritis combined with contralateral nephrectomy 7 days later. The aneurysms distributed throughout the brain and iris were studied by microradiography; a few representative aneurysms selected from the microradiographs were studied histologically. The microradiographic findings and histological sections correlated well. Intracranial microaneurysms were multiple and frequently located in the basal ganglia and near the cortex. Arterial changes in the iris paralleled intracranial arterial changes in degree and type except for the addition of hemorrhage around some microaneurysms. The results of this study show the potential of microradiography and histological sections guided by microradiography for studying the natural history of hypertensive arterial lesions and support the contention that hypertension, microaneurysms and intracerebral hemorrhages are related.
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PMID:Microradiographic study of cerebral and ocular aneurysms in hypertensive rabbits. 64 69

Cellophane perinephritis hypertension was produced in four dogs, while five additional dogs served as normotensive controls. A competitive antagonist of angiotensin II, 1-sarcosine-8-alanine angiotensin II, was infused iv into these conscious dogs at a rate of 6 mug/min/kg of body weight for 45 min. Arterial pressure averaged 170 +/- 11 (SEM) mm Hg in the dogs with perinephritic hypertension, and was not altered significantly during infusion of the angiotensin antagonist. In the normal dogs the arterial pressure averaged 100 +/- 10 mm Hg and likewise, did not change during administration of the angiotensin analog. Plasma renin activity values were essentially the same in these two groups of dogs and did not change during infusion of the angiotensin antagonist. These studies provide strong evidence that the renin-angiotensin system is not involved in maintaining the elevated arterial pressure in dogs with chronic hypertension produced by cellophane perinephritis.
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PMID:Role of the renin-angiotensin system in dogs with perinephritis hypertension. 96 86

Total inositol phosphate (IP) formation was measured in the aorta and femoral artery from rabbits at 1, 2, and 6 weeks after kidney wrapping, at which times the mean arterial pressures were 88 +/- 4, 96 +/- 3 and 126 +/- 7 (control = 74 +/- 3) mmHg. Noradrenaline (10(-7)-10(-4) M)-stimulated IP formation was increased in the aorta and femoral artery from hypertensive rabbits at 2 weeks (e.g., aorta noradrenaline 10(-6) M sham = 105 +/- 14%, hypertensive = 164 +/- 20% of control). In contrast, endothelin-1-stimulated IP formation was unchanged at 2 weeks. Noradrenaline-stimulated IP formation was unchanged at 1 and 6 weeks. Basal IP formation was not significantly different in normotensive and hypertensive animals. In perinephritis hypertension, there is an alteration in phosphatidylinositol metabolism in arterial smooth muscle at the time when blood pressure is rising rapidly. This alteration may affect a specific phosphatidylinositol pool that is linked to the alpha-adrenoceptor but not to the endothelin-1 receptor.
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PMID:Noradrenaline and endothelin-stimulated inositol phosphate formation in arterial smooth muscle from rabbits with perinephritis hypertension. 179 9

Total inositol phosphate formation was measured in the aorta and femoral artery from rabbits at 1, 2 and 6 weeks after kidney wrapping, at which times the mean arterial pressures were 88 +/- 4, 96 +/- 3 and 126 +/- 7 mmHg against a control pressure of 74 +/- 3 mmHg. Noradrenaline-stimulated (10(-7) to 10(-4) mol/l) inositol phosphate formation was increased in the aorta and femoral artery from hypertensive rabbits at 2 weeks (aorta noradrenaline 10(-6) mol/l sham, 105 +/- 14%; hypertensive, 164 +/- 20% of control). Noradrenaline-stimulated inositol phosphate formation was unchanged at 1 and 6 weeks in the aorta. Endothelin-stimulated inositol phosphate formation was unchanged at 2 weeks. Basal inositol phosphate formation was not significantly different in normotensive and hypertensive animals. In perinephritis hypertension there is an alteration in phosphatidylinositol metabolism in arterial smooth muscle. This occurs at the time when the blood pressure is rising rapidly. This alteration may affect a specific phosphatidylinositol pool that is linked to the alpha-adrenoceptor but not to the endothelin receptor.
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PMID:Inositol phosphate formation in arterial smooth muscle from rabbits with perinephritis hypertension. 196 6

1. Contractions of isolated vascular and cardiac preparations taken from rabbits with perinephritis (one kidney, one wrapped) hypertension were compared with those of preparations from control operated animals. 2. Significantly increased sensitivity to noradrenaline, which acts on alpha 1-adrenoceptors, was found in mesenteric arterial rings but not in aortic rings. The degree of hypersensitivity was the same in the presence and absence of cocaine, suggesting that there is no increase in uptake of noradrenaline into adrenergic nerves in this model of hypertension. In contrast to these agonist-induced contractions, no increased sensitivity was found to potassium chloride, suggesting that hypersensitivity is specific for receptor mediated rather than membrane potential mediated effects. 3. No hypersensitivity to noradrenaline was found in the isolated left or right atria, which suggests that the hypertension is associated with changes in excitation-contraction coupling in blood vessels but not in cardiac muscle. 4. Hypertension increased basal 45Ca uptake in the mesenteric artery but not in the aorta. However, there was no significant difference between preparations from normotensive and hypertensive rabbits in 45Ca uptake or efflux stimulated by noradrenaline or KCl. 5. Increased basal 45Ca uptake could contribute to the increased sensitivity to noradrenaline found in the mesenteric artery in rabbit perinephritis hypertension.
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PMID:Noradrenaline sensitivity and calcium fluxes in arteries from rabbits with perinephritis hypertension. 220 98

The present study was undertaken to investigate beta-adrenoceptor-adenylate cyclase coupling in a myocardial ventricular membrane preparation and in isolated renal glomeruli of cellophane perinephritis hypertensive rats. Adenylate cyclase activity and [125I]iodocyanopindolol binding were differentially affected in these preparations. In isolated glomeruli of hypertensive rats a reduced intrinsic activity of isoproterenol was associated with an apparent loss of the guanine nucleotide-sensitive high-affinity state of the beta-adrenoceptors, whereas their absolute number was unchanged when compared with the normotensive control rats. On the other hand, in the sarcolemmal preparation of hypertensive rats adenylate cyclase activity, the relative amount of high-affinity states, and the density of beta-adrenoceptors were not different from the respective values in normotensive controls. Experiments performed on isolated glomeruli of rats with unilateral cellophane perinephritis that developed only moderate hypertension provide evidence that the apparent loss of the high-affinity state is a consequence of hypertension, since no difference was observed in glomeruli from the wrapped, as compared with the intact kidney.
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PMID:Alterations of the glomerular beta-adrenoceptor-linked adenylate cyclase system in perinephritis hypertension. 241 95

The effects of perinephritis hypertension on lymphocyte and cardiac beta-adrenoceptors in the rabbit were examined. Hypertensive animals 8-12 weeks after surgery had an increase in cardiac weight consistent with hypertrophy compared with sham-operated age-matched controls. Specific binding of [I125] iodocyanopindolol (ICYP) to cardiac ventricular membranes was reduced in the hypertensive animals (Bmax44 +/- 14 in hypertensives and 30 +/- 15 fmoles/mg protein in controls; p less than 0.01). However, weight-matched ventricles from a group of older sham-operated normotensive rabbits showed a similar cardiac beta-receptor number to that found in the hypertensive animals. There were no changes in affinity of the ligand for the binding site. The reduction in cardiac beta-receptor density was not accompanied by changes in the chronotropic or blood pressure responses to isoprenaline in the conscious animal. Specific ICYP binding to lymphocyte beta-receptors did not differ significantly between the hypertensive and age-matched normotensive animals. Lymphocyte beta-adrenoceptors thus may not always reflect changes in heart beta-adrenoceptors, and changes in receptor density may not be directly related to blood pressure or have identifiable functional significance.
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PMID:Cardiac and lymphocyte beta-adrenoceptors in perinephritis hypertension in the rabbit. 242 74

A comparison was made of contractile responses of aortic rings isolated from rabbits with perinephritis hypertension and sham-operated rabbits. Contraction was elicited by potassium, noradrenaline or 11,9-epoxymethano PGH2 (a thromboxane A2 mimetic). Except for the maximum response to noradrenaline, there were no significant differences in the responses to KCl or 11,9-epoxymethano PGH2 between normotensive and hypertensive rabbit aorta preparations. Hypertensive rabbit aorta preparations were more susceptible to the calcium channel inhibitors nifedipine and nisoldipine, but less sensitive to a calcium channel facilitator Bay K 8644 than were normotensive preparations. These results suggest that calcium regulatory mechanisms undergo changes during the development of hypertension. We have also found that nifedipine and nisoldipine show high inhibitory potency in the calcium channel inhibitor-sensitive contractile component during alpha-adrenoceptor activation and appear to be weak competitive antagonists at thromboxane A2 receptor sites.
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PMID:Effects of drugs that activate or inhibit calcium channels on contraction of the aorta from hypertensive rabbits. 243 44

Uptake of 45Ca was measured in rings of thoracic aorta from rabbits with hypertension, induced by cellophane perinephritis (Page hypertension: one-kidney, one wrap). Basal 45Ca uptake was increased significantly in the hypertensive group (sham: 100 +/- 3, hypertensive: 133 +/- 11 nmol/g wet weight, n = 6). 45Ca uptake was increased by KCl (30 mmol/l), norepinephrine (50 nmol/l) and Bay K 8644 (14 or 56 nmol/l) by the following amounts: 152, 15, 28 and 36%, respectively. Stimulated 45Ca uptake was less in hypertensive animals for all agonists. The augmenting effect of Bay K 8644 on 45Ca uptake, stimulated by norepinephrine or by KCl, was also reduced in hypertension. It is concluded that in hypertension there are alterations in the Ca regulatory process and in the properties of the Ca channel in arterial muscle.
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PMID:45Ca uptake and the actions of Bay K 8644 on aortic strips from rabbits with perinephritis hypertension. 244 70


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