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

We investigated pressor sensitivity to infused phenylephrine (PE), 0.05 to 0.4 micrograms/kg/min, and angiotensin II (Ang II), 2.5 to 10 ng/kg/min, in 35 patients with mild-to-moderate hypertension, before and at the end of a 4-week treatment period with the angiotensin-converting enzyme (ACE) inhibitor, cilazapril, 2.5 or 5.0 mg/day. Cilazapril lowered the mean systolic and diastolic blood pressure by 10.6/3.5 mm Hg, but had no effect on the dose-response curves of dose of PE or Ang II vs. the increase in systolic, diastolic, or mean blood pressure, or heart rate. There were also no significant effects of cilazapril on PD20 values, i.e., the dose of PE or Ang II required to increase mean arterial blood pressure (MAP) by 20 mm Hg, or on delta R-R/delta MAP (ratio of the increase of the ECG R-R interval to the increase in mean arterial blood pressure) as a measure of baroreflex sensitivity. Plasma renin activity was significantly increased by cilazapril therapy, but there were no changes in plasma concentrations of Ang II or atrial natriuretic factor. We conclude that cilazapril, an ACE inhibitor, does not alter alpha 1-adrenoceptor and Ang II receptor sensitivity to selective agonists, nor does it affect baroreflex sensitivity.
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PMID:Alpha-adrenergic and angiotensin II pressor sensitivity in hypertensive patients treated with an angiotensin-converting enzyme inhibitor. 138 57

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

Calcium entry blockade may affect the pressor reactivity to vasoconstrictors. The pressor response to norepinephrine and angiotensin II, as well as several other blood pressure modulating factors, were studied in normal subjects (n = 9) and patients with essential hypertension (n = 10) before and after 8 weeks of treatment with the long-acting dihydropyridine amlodipine. In control subjects, calcium entry blockade did not modify blood pressure, the pressor and aldosterone response to angiotensin II, the activity of the renin-angiotensin and sympathetic nervous systems, or urinary dinoprostone (prostaglandin E2) excretion; however, the pressor response to norepinephrine was significantly decreased (p less than 0.01). In patients with hypertension, amlodipine decreased blood pressure (p less than 0.01) and the pressor response to both norepinephrine and angiotensin II (p less than 0.01), without changes in body weight, plasma renin, angiotensin II and catecholamine levels, dinoprostone excretion, or aldosterone responsiveness to angiotensin II. These findings suggest that calcium entry blockade modifies sympathetic-dependent vasoconstriction in both normal subjects and in patients with hypertension. Angiotensin II pressor response may be selectively decreased in essential hypertension.
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PMID:Antihypertensive mechanism of amlodipine in essential hypertension: role of pressor reactivity to norepinephrine and angiotensin II. 138 65

Losartan, a recently developed nonpeptide angiotensin II (Ang II) receptor antagonist, was administered orally to 10-week-old spontaneously hypertensive rats (SHR) for 2 weeks. Cardiac weight and tissue Ang II, as well as plasma renin activity (PRA) and Ang II, were determined. Treatment with Losartan (10 mg/kg per day) lowered blood pressure markedly. Losartan reduced significantly the left ventricular weight by 11% compared with control rats. The left ventricular Ang II content was lowered by Losartan (18.6 +/- 0.9 pg/tissue; 21.9 +/- 0.9 pg/tissue, control, p less than 0.05), whereas PRA and plasma Ang II concentration were increased by the treatment. With the control and Losartan-treated animals, there was a significant positive correlation between the left ventricular weight and the tissue Ang II content (r = 0.563, p less than 0.05). These results provide evidence that cardiac tissue Ang II, rather than circulating Ang II, plays an important role in the pathophysiology of left ventricular hypertrophy of this animal model of human hypertension.
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PMID:Effects of losartan, a nonpeptide angiotensin II receptor antagonist, on cardiac hypertrophy and the tissue angiotensin II content in spontaneously hypertensive rats. 138 40

Angiotensin II (Ang II) in low dose raises blood pressure slowly by a mechanism which is not understood, but which is clearly different from the better known direct vasoconstrictor effect. Vascular hypertrophy develops during this slow pressor response, but is not wholly a consequence of the increase of pressure. We discuss non-pressor mechanisms by which Ang II may act as a growth factor to promote structural vascular change. Studies with cultured vascular smooth muscle cells suggest at least three possibilities, but none of these has been tested in vivo during slow pressor infusion of Ang II. The action of growth factors may be important in hypertension since increased arterial pressure causes vascular hypertrophy. Growth factors influence markedly the extent of this hypertrophic response and, however produced, vascular hypertrophy has an important influence on resistance and arterial pressure in hypertension.
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PMID:Angiotensin II, vascular structure and blood pressure. 138 40

We cultured smooth muscle cells from rat renal preglomerular arterioles by injecting a suspension of iron oxide into the left ventricle, separating the arterioles magnetically, and growing cells from explants. In passaged cultures we ascertained vascular smooth muscle purity of > 98% by morphology; contraction to norepinephrine and angiotensin; positive immunofluorescence staining through the sixth passage with monoclonal antibodies to smooth muscle-specific alpha- and gamma-isoactins, myosin, and desmin; and the absence of von Willebrand factor. Angiotensin II (10(-12)-10(-5) M) induced dose-dependent DNA synthesis and proliferation of subcultured (three times) arteriolar smooth muscle cells from a growth-arrested state (p < 0.01). Angiotensin II (10(-5) M) also induced the cells to express c-fos mRNA. We find no previous report of culture of smooth muscle cells from renal preglomerular arterioles. Our findings also provide evidence that angiotensin II is mitogenic to arteriolar muscle cells and thus may be involved in their hyperplasia accompanying hypertension.
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PMID:Culture of renal arteriolar smooth muscle cells. Mitogenic responses to angiotensin II. 139 76

MK 954 (DuP 753), a recently developed angiotensin II (Ang II) receptor antagonist, was administered orally for 2 weeks to spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Whereas the basal levels of plasma Ang II were lower in SHR than in WKY, treatment with MK 954 markedly reduced blood pressure in SHR but not in WKY. Plasma renin activity, Ang I and Ang II were increased, while plasma aldosterone was decreased in both strains. These results no only indicate therapeutic efficacy of this agent in the chronic treatment of human hypertension, but also support the idea that the renin-angiotensin system plays an important role in the control of blood pressure in SHR.
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PMID:Antihypertensive and hormonal activity of MK 954 in spontaneously hypertensive rats. 139 95

Women with pregnancy-induced hypertension (PIH) are characterized by relatively greater blood pressure sensitivity to exogenous angiotensin II (Ang II) than normotensive pregnant women. Evidence suggests that this is due to an alteration in Ang II receptor sites. However, the question of whether this represents an increase in receptor number or affinity remains unanswered. To answer this question Ang II receptors on platelets from normotensive women during each trimester of pregnancy and the postpartum period were studied and compared with platelet Ang II binding in third trimester women with PIH and in postpartum women who had had a recent pregnancy complicated by PIH. We also measured plasma renin activity, Ang II, and aldosterone in blood samples from these women and sodium and creatinine in 24-hour urine collections. Normotensive pregnant women had significantly less platelet Ang II binding than nonpregnant, postpartum women (0.85 +/- 0.19 versus 2.87 +/- 0.83%, p = 0.003), reflecting a reduction in receptor number but not affinity. This probably reflects the significant increase in Ang II during pregnancy. Urinary sodium excretion was equivalent and could not explain these changes. Comparisons of third trimester women with PIH against those without PIH documented a significantly higher Ang II binding in the women with PIH (2.23 +/- 0.42 versus 0.85 +/- 0.19%) that was caused by an increase in receptor number (6.0 +/- 1.3 versus 3.0 +/- 0.8 fmol Ang II per 5.6 x 10(8) platelets, p = 0.047) but similar Ang II binding affinity. This reflected significantly lower Ang II levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Nov
PMID:Increased platelet angiotensin II receptor number in pregnancy-induced hypertension. 142 14

Angiotensin II-induced phosphorylation of proteins was examined in isolated myocytes from hearts of Dahl rats. A high salt diet induced cardiac hypertrophy in Dahl salt-sensitive rats. Angiotensin II-induced phosphorylation of a 42-kd protein (pp42) was detected by two-dimensional electrophoresis in hypertrophic but not normal ventricular myocytes. Angiotensin II stimulation was time-dependent, with a peak effect at 30 minutes. The half-maximal and maximal concentrations of angiotensin II that stimulated pp42 phosphorylation were 1 and 10 nM, respectively. Phosphorylation of pp42 was a function of cardiac hypertrophy. Phorbol 12-myristate 13-acetate-induced phosphorylation of pp42 indicates the possibility of an association between protein kinase C and the signal transduction pathway of angiotensin II-induced pp42 phosphorylation. Ionomycin and A23187 (both at 1 microM) did not stimulate phosphorylation of pp42. Angiotensin II produced a small increase in the synthesis of myocyte proteins in both normal and hypertrophic cells as shown by [35S]methionine incorporation. However, this increase could not account for the increase in the phosphate content of pp42. This protein was not an isoform of actin nor was it of platelet origin. These results raise the possibility that angiotensin II may play a role in the activation of factors in hypertrophic myocytes; however, further study is required to define a link between phosphorylation of pp42 and the hypertrophic process.
Hypertension 1992 Nov
PMID:Angiotensin II-induced protein phosphorylation in the hypertrophic heart of the Dahl rat. 142 15

We studied the influence of nicardipine on renin-angiotensin (RA) system in twelve elderly patients, because the suppression of RA system, the decrease in reactivity of its feedback mechanism, and a high probability of arteriosclerosis and hypertension are well recognized in elderly patients. In hypertensive crisis during operation, intravenous bolus injection of nicardipine was done promptly by anesthesiologists in charge. Plasma renin activity (PRA), angiotensin I (A I), and angiotensin II (A II) were measured with RIA methods before administration of nicardipine and after hemodynamics were stabilized. Changes of systemic arterial pressure and heart rate were simultaneously recorded. Concentrations of PRA, A I, and A II were not significantly elevated, whereas systemic and diastolic blood pressures decreased significantly at 5 min, 15 min, 30 min and 60 min after administration of nicardipine. Heart rate was unchanged. But in a few cases there was an increase in PRA and A I. Average total dose of nicardipine was 26.8 micrograms.kg-1 and average fall of blood pressure was 23.9%. In conclusion, we can use intravenous nicardipine safely and stabilize hemodynamics easily without activation of RA system and rebounding of its feedback mechanism.
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PMID:[Influence of nicardipine on the renin-angiotensin system ina hypertensive crisis during operation in elderly patients]. 143 43


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