Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve women in their first 3 months of pregnancy received an i.v. saline load (3 mmol sodium/kg) and a graded infusion of angiotensin II (Ang II; i.e. 4, 8 and 16 ng/kg per min). As controls, twelve comparable pregnant subjects received the saline infusion alone. Eight non-pregnant women underwent both protocols, with doses of 2, 4 and 8 ng/kg per min Ang II, and thus acted as their own controls. Saline loading evoked proportionately similar falls in basal plasma renin (PRC) and plasma aldosterone (PAC) concentrations in pregnant and non-pregnant women. Angiotensin II evoked a dose-dependent pressor response, a graded increase in PAC and a reduction in sodium and urate excretion in both pregnant and non-pregnant women. The administration of Ang II had a proportionately greater effect on sodium and urate excretion in non-pregnant than in pregnant women; the pressor response to Ang II was also decreased in the pregnant women. The stimulation of PAC by Ang II, however, did not differ between the two groups. These results show that refractoriness to the renal and vascular effects of Ang II is present as early as the eleventh week of gestation. They also support the hypothesis that there is a degree of dissociation between the renin-angiotensin system and PAC in normal pregnancy.
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PMID:The effects of intravenous angiotensin II upon blood pressure and sodium and urate excretion in human pregnancy. 341 Nov 23

Dose-response curves of blood pressure and of the biochemical components of the renin-angiotensin-aldosterone system were determined during long-term treatment with captopril in 21 hypertensive patients. Captopril was given in biweekly, doubling doses starting with 25 mg 3 times a day until control of blood pressure was achieved or a total daily dosage of 600 mg was reached. Recumbent and standing systolic and diastolic blood pressure fell on 75 mg captopril daily. Increasing the captopril dose did not induce further significant hypotensive effects. The pretreatment level of plasma renin activity (PRA) was a poor predictor of the hypotensive effect of captopril. The rises in PRA and plasma angiotensin I level (PA I) and the decrease in plasma angiotensin II level (PA II) and plasma aldosterone level (PAC) provide biochemical evidence for angiotensin-converting enzyme (ACE) inhibition in vivo. These effects were present on daily doses of 75 to 150 mg captopril.
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PMID:Dose response in captopril therapy of hypertension. 625 Jul 59

We compared the effects of 500 ml of 0.15M NaCl or 750 ml of 0.15M NaHCO2, infusions on PRA and PAC in 16 normal NaCl-restricted men. More positive sodium balance, greater natriuresis, and lower serum chloride, potassium, and hydrogen ion concentrations were observed after NaHCO3 infusion. PRA decreased (13.8 +/- 1.0 ng/ml angiotensin I per hour to 6.6 +/- 0.70) and PAC did not change (98 +/- 15 ng/dl to 86 +/- 15) after NaCl infusion. Conversely, PRA did not change (9.9 +/- 1.6 to 10.1 +/- 1.6) and PAC decreased (85 +/- 9 to 44 +/- 5) after NaHCO3 infusion. Plasma cortisol declined in both groups. These results suggest that in sodium-restricted man chloride is more important than sodium for the suppression of PRA by NaCl loading and that potassium or hydrogen ion is a more sensitive modulator of aldosterone secretion than is renin.
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PMID:Renin and aldosterone responses to short-term NaCl or NaHCO3 loading in man. 628 47

An interaction between angiotensin II (Ang II) receptors and alpha 2-adrenoceptors was evaluated in the nucleus tractus solitarii (NTS) of the normotensive Wistar-Kyoto rat (WKY) and of the spontaneously hypertensive rat (SHR) using quantitative receptor autoradiography and cardiovascular analysis. In the WKY rat, Ang II promoted a dose-dependent increase in the IC50 value of l-noradrenaline when competing for ([3H]p-aminoclonidine ([3H]PAC) binding sites, which reached a maximum of 400% with 10 nM of Ang II and was associated with a small decrease in the B0 value (20%). In the SHR Ang II (0.1 nM) had an opposite effect leading to a decrease in the IC50 value of about 57%, and no change was observed in the B0 value. Saturation analysis also showed that Ang II (0.1 nM) increased the KD value of [3H]PAC in the WKY strain but in contrast decreased the KD value of [3H]PAC in the SHR. The Bmax value was not significantly changed neither in the WKY rat nor in the SHR. The cardiovascular analysis showed that a threshold dose of Ang II (0.05 pmol) counteracted the vasodepressor effect produced by l-noradrenaline coinjected in the NTS of the WKY rat. No effect was observed in heart rate. In the SHR no counteraction of the l-noradrenaline-induced vasodepressor effect was found, and in contrast a slight increase of the vasodepressor effect associated with a significant increase in the bradycardiac response was observed. The results give evidence for an antagonistic Ang II/alpha 2 receptor interaction in the cardiovascular part of the NTS of the WKY rat as previously observed in the Sprague-Dawley rat. However, this interaction is altered in the SHR, so that in this strain the Ang II/alpha 2 receptor interaction enhances alpha 2 affinity and possibly alpha 2 receptor function. This opposite effect observed in the SHR may represent one compensatory mechanism to counteract the development of high blood pressure in the SHR.
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PMID:Evidence for a differential modulation of the alpha-2 adrenoceptors by angiotensin II in the nucleus tractus solitarii of the spontaneously hypertensive and the Wistar-Kyoto normotensive rats. 764 60

"Non-modulators" are essential hypertensive patients who fail to modulate an adrenal response, renovascular response, or both, to angiotensin II (Ang II). The aim of the present study was to characterize "non-modulators" among Japanese patients with normal-renin essential hypertension and to determine whether non-modulation is related to sodium sensitivity of blood pressure. The increase in plasma aldosterone concentration (PAC response) and the decrease in renal plasma flow (RPF response) in response to Ang II infusion (3 ng/kg/min) were assessed in 15 Japanese patients with essential hypertension who received a high sodium diet (250 mEq/d) followed by a low sodium diet (10 mEq/d). The subjects were divided into two groups (6 modulators and 9 non-modulators) based on their ability to modulate the PAC response during sodium restriction. There was no significant difference between modulators and non-modulators in electrolyte balance or in plasma Ang II levels on either diet. Changes in the PAC response during sodium restriction were significantly correlated with the change in mean blood pressure during sodium restriction (r = -0.67, p < 0.01), while changes in the RPF response were not. RPF responses in both groups decreased during sodium restriction, although an effect on the RPF response in non-modulators was unexpected. These results suggest that non-modulators do exist among Japanese patients, but that this defect does not involve both the adrenal gland and the kidney. Apparently, only non-modulation of the adrenal response is involved in the mechanism of sodium sensitivity.
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PMID:Modulation of target tissue response to angiotensin II and sodium sensitivity in Japanese patients with essential hypertension. 889 41

Catecholamines, neuropeptide Y (NPY) and angiotensin II (Ang II) are known to participate in the central control of blood pressure. However, the modulation of these neurotransmitter receptors in response to a hypertensive stimulus is not appropriately established. The purpose of the present study was to examine binding parameters of alpha(2)-adrenergic, NPY and Ang II receptors in the nucleus tractus solitarii (NTS) and paraventricular hypothalamic nucleus (PVN) following a hypertensive stimulus in the aortic-coarcted rat by means of quantitative receptor autoradiography. No changes were seen in binding parameters of alpha(2)-adrenergic and NPY receptors in the NTS of the hypertensive rat compared to control. However, an increased affinity (54%) of noradrenaline competing for 3H-PAC was seen in the PVN. Moreover, an increased binding (49%) of 125I-PYY was also observed in the PVN. The affinity of Ang II for 125I-Sar(1)Ile(8)-Ang II binding sites was also increased (57%) in the NTS of the hypertensive rat. No changes in the binding parameters of radioactive Ang II were observed in the PVN. The results suggest that systems involved with hypertension like Ang II in the NTS and catecholamines in the PVN might collaborate in the development/maintenance of high blood pressure in the aortic-coarcted rat.
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PMID:Quantitative autoradiography of adrenergic, neuropeptide Y and angiotensin II receptors in the nucleus tractus solitarii and hypothalamus of rats with experimental hypertension. 1136 90