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

The effects of an angiotensin-II analog (saralasin, i.v.) and of a converting enzyme inhibitor (captopril, oral) were compared in 12 sodium-depleted patients with hypertension. The decrease of the mean intraarterial pressure (MAP) with captopril (-21.5 +/- [SEM] 4.3 mm Hg) was more pronounced (P < 0.001) than the change of MAP during saralasin (-10.5 +/- 4.0 mm Hg). The pretreatment arterial plasma renin activity (log PRA) was closely related to the change of MAP during saralasin (r = -0.94; P < 0.001) and also to the captopril-induced change of MAP (r = -0.82; P < 0.001); similar results were obtained for the log plasma angiotensin (PA) I and II levels. The change of MAP was more pronounced, however, with captopril than during saralasin at any level of pretreatment PRA, PAI or PAII. Saralasin did not affect heart rate (P > 0.4), but during captopril the heart rate increased by 5.1 beats/min (P < 0.001). Captopril produced a 70% decrease of PAII, but the change of MAP was poorly related to the changes of PAII (r = -0.57; P < 0.05); PRA and PAI rose threefold to fourfold. PRA, PAI, and PAII all increased during saralasin. These observations may suggest that the antihypertensive action of captopril is not based solely on the inhibition of AII formation, but also the agonistic effect of saralasin has to be considered.
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PMID:Comparative study of an angiotensin-II analog and a converting enzyme inhibitor. 624 56

Liddle's syndrome was diagnosed in a 23-yr-old Chinese girl with hypertension and hypokalemia by the presence of suppressed renin and negligible plasma and urinary aldosterone secretion. Adrenal corticosteroids, including aldosterone, were suppressed by dexamethasone and stimulated by ACTH. While spironolactone was ineffective, triamterene (2,4,7-triamino-6-phenyl-pteridine) treatment corrected the hypertension and hypokalemia and restored PRA to normal provided that sodium intake was not excessive. During long term treatment with triamterene, blood pressure was extremely sensitive to salt intake, increasing promptly with high intake and decreasing with low salt intake. As a result of the chronic hypervolemia and sodium retention consequent upon the patient's persistent high salt intake and increased renal tubular sodium reabsorption, plasma renin and aldosterone remained low. Erythrocyte sodium concentration and membrane permeability were increased. Triamterene with salt restriction was able to lower the intracellular sodium concentration but did not correct the increased sodium permeability. This suggests that there is an abnormality of sodium transport in Liddle's syndrome which affects the erythrocytes as well as the renal tubular cells.
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PMID:The effect of triamterene and sodium intake on renin, aldosterone, and erythrocyte sodium transport in Liddle's syndrome. 626 54

Dexamethasone suppressed urinary aldosterone to less than 1.5 micrograms/day in 1-2 days and lowered blood pressure in a woman and in her 2 1/2-yr-old daughter, both of whom have hypertension and hyporeninemia and are members of a kindred with dexamethasone-suppressible aldosteronism. ACTH given for 7 days produced a sustained increase in aldosterone production and a rise in blood pressure in both patients. The abnormal suppression with dexamethasone and further stimulation with ACTH indicate that the aldosteronism is ACTH-dependent in this disorder. The cause of the ACTH-dependence of aldosterone production in this disorder is unknown but may represent continued stimulation rather than the usual (secondary) inhibition by ACTH of 11-hydroxylation and 18-hydroxylation in zone glomerulosa cells. Blood pressure was normal during treatment with spironolactone and during pregnancy, when the action of aldosterone and other similar steroids was presumably blocked by an increased production of progesterone; this suggests that the hypertension is dependent upon sodium-retaining steroids such as aldosterone. Aminoglutethimide given during treatment with ACTH decreased urinary aldosterone and blood pressure and increased PRA, with minimal effects on plasma cortisol or urinary 17-hydroxycorticosteroids. These results provide additional evidence that aldosterone, acting alone or in conjunction with other steroids synthesized by the zona glomerulosa, mediates the hypertension and hyporeninemia of dexamethasone-suppressible aldosteronism.
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PMID:Overproduction of sodium-retaining steroids by the zona glomerulosa is adrenocorticotropin-dependent and mediates hypertension in dexamethasone-suppressible aldosteronism. 626 87

Hormonal and mean arterial pressure (MAP) responses to posture, isometric handgrip, angiotensin II (AII), adrenocorticotrophic hormone (ACTH), and metoclopramide (MCP), a dopamine (DA) antagonist, were examined in nine men with essential hypertension and nine age- and weight-matched normotensive men on a constant 100 mEq sodium and 80 mEq potassium intake before and after 4 days of administration of the DA agonist, bromocriptine (BEC; 2.5 mg three times a day). BEC depressed supine basal MAP in the hypertensives, and decreased MAP response to posture and isometric exercise in both groups. Hypertensives displayed greater (p less than 0.01) NE responses to posture and exercise than the normotensives. BEC decreased the NE response to 10 minutes of upright posture and exercise more in hypertensives (p less than 0.01) than in normotensives, but following BEC, the responses were similar. BEC did not affect basal PRA or PRA responses to posture and exercise in the two groups. PA responses to ACTH and MCP were similar in both groups, but the hypertensives displayed greater (p less than 0.01) PA responses to AII. BEC suppressed PA responses to AII (p less than 0.01) and to high dose ACTH (p less than 0.05) to a similar extent in both groups. The prolactin as well as the PA response to DA antagonism with MCP was similar in the two groups. These results suggest that dopaminergic control of NE secretion may be altered in essential hypertension. Blood pressure lowering effects of BEC in patients with essential hypertension may be related, in part, to depression of sympathetic nervous system activity.
Hypertension
PMID:Dopaminergic modulation of pressor and hormonal responses in essential hypertension. 627 98

The chronic effects of ACTH on mean arterial pressure (MAP) and related variables were studied in dogs with both chronic norepinephrine (NE)- and chronic aldosterone-induced hypertension. MAP was recorded continuously for 24 hours/day, and sodium intake was 71 mEq/day. ACTH was infused for 8 days at a rate that does not increase MAP in normotensive dogs and yet a rate that produces pronounced mineralocorticoid and glucocorticoid effects. Chronic ACTH infusion in dogs with NE hypertension caused natriuresis, kaliuresis, diuresis, hypernatremia, hypokalemia, and suppression of PRA; additionally, there was either no net change in water balance or net water balance was positive. However, in marked contrast to dogs without pre-existing hypertension, in dogs with NE hypertension ACTH produced a pronounced additional increase in MAP of 39 to 63 mm Hg. Although ACTH markedly potentiated NE hypertension, high infusion rates of aldosterone (+6 mm Hg) and cortisol (-7 mm Hg) had relatively weak effects on MAP; further, in dogs with NE hypertension, the increase in MAP associated with simultaneous infusions of high rates of cortisol and aldosterone was equal to only approximately half of that produced by ACTH. In dogs with aldosterone hypertension, the changes in salt and water balance produced by ACTH were comparable to those that occurred when ACTH was administered to dogs with NE hypertension. In dogs with aldosterone hypertension, however, ACTH did not produce kaliuresis, hypernatremia, or hypokalemia; moreover, ACTH did not exacerbate aldosterone hypertension. Thus, the data indicate that the hypertensive effects of ACTH are manifested in conditions of reduced renal excretory capacity such as exist when plasma levels of the potent sodium -retaining hormone NE are inappropriately elevated. Finally, the hypertensive effects of ACTH cannot be accounted for simply on the basis of enhanced mineralocorticoid and glucocorticoid activity.
Hypertension
PMID:Chronic potentiation of vasoconstrictor hypertension by adrenocorticotropic hormone. 627 99

19-Nor-deoxycorticosterone (19-nor-DOC) is a naturally occurring, potent mineralocorticoid present in hypertensive animal models as well as man. To investigate 19-nor-DOC's regulation and possible pathogenesis in hypertension, urinary free (UF) 19-nor-DOC was measured in 14 hypertensives, correlated with other corticosteroids and systemic arterial blood pressure (BP), and compared to basal and ACTH-stimulated values in 8 normotensive subjects. Seven of the 14 hypertensives had low-renin hypertension, 2 had primary aldosteronism, 1 had an adrenal carcinoma, and another had acromegaly. These studies determined that: 1) although the mean UF 19-nor-DOC was not increased in hypertensives (588 +/- 180 vs. 428 +/- 122 ng/day), 2 low-renin hypertensives had quite elevated levels (2186 and 2018); 2) the UF 19-nor-DOC in hypertensives was correlated with BP but not with PRA, aldosterone secretion, plasma potassium, basal plasma cortisol, or 17-hydroxycorticosteroids; 3) likewise, in normotensives, UF 19-nor-DOC did not correlate with basal plasma cortisol, cortisol secretion, or 17-hydroxycorticosteroids excretion but did correlate after ACTH stimulation. Therefore, although 19-nor-DOC is activated by ACTH administration, it is not correlated with basal parameters of cortisol production, suggesting that factors other than ACTH regulate basal 19-nor-DOC secretion. Furthermore 19-nor-DOC is elevated in some hypertensive patients, and it is directly related to the elevation of mean systemic BP. This suggests that, although 19-nor-DOC could contribute to hypertensive disease in some individuals, it does not appear to be due to excess ACTH.
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PMID:The regulation of urinary free 19-nor-deoxycorticosterone and its relation to systemic arterial blood pressure in normotensive and hypertensive subjects. 629 58

This is the first autopsy case of male 17 alpha-hydroxylase deficiency with malignant hypertension. The subject had hypertension, hypokalemic alkalosis, and pseudohermaphroditism. At age 21, 17 alpha-hydroxylase deficiency was diagnosed by low urinary excretion of 17-hydroxysteroids, low secretion rate of cortisol, and low plasma testosterone level in association with high urinary excretion of pregnanediol and high plasma progesterone and corticosterone. Urinary excretion of aldosterone and PRA were suppressed, and plasma ACTH was elevated. Hypertension and hypokalemic alkalosis were normalized with dexamethasone therapy. After missing 5 yr of follow-up, malignant hypertension developed, and PRA and aldosterone were elevated. Histological examination revealed some characteristic arteriolar lesions as in malignant nephrosclerosis. Juxtaglomerular hyperplasia and an increase of renin granules were observed, which reflected high PRA. Abnormal histological findings of endocrine organs were observed in the breast, the pituitary gland, the adrenal glands, and the testis.
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PMID:An autopsy case of 17 alpha-hydroxylase deficiency with malignant hypertension. 630 Jan 76

To determine the contribution of receptor number and affinity to changes in vascular reactivity to angiotensin II (AII) in hypertensive rats, we have investigated the binding of 125I-AII to a particulate fraction of the rat mesenteric artery of hypertensive rats. In two-kidney, one clip hypertensive rats, receptor concentration (Bmax) was 83 +/- 13 fmol/mg and the dissociation constant (Kd) 0.6 +/- 0.1 nM vs 75 +/- 5.3 fmol/mg and 0.6 +/- 0.1 nM in normotensive controls, although PRA was much higher in the former. Bmax was reduced in these hypertensive rats after sodium depletion, as in normal rats. One-kidney, one clip hypertensive rats (Bmax 88 +/- 17 fmol/mg, Kd 0.6 +/- 0.1 nM) did not differ from uninephrectomized control rats (96 +/- 9 fmol/mg, Kd 0.5 +/- 0.1 nM). In DOCA-salt hypertensive rats, binding capacity was increased (125 +/- 2 fmol/mg, Kd 0.7 +/- 0.0 nM) vs uninephrectomized salt-loaded rats (Bmax 95 +/- 6 fmol/mg, Kd 0.6 +/- 0.1 nM), although PRA was suppressed comparably in both groups. The salt-loaded rats did not differ from uninephrectomized controls drinking water. We conclude that changes in the circulating renin-angiotensin system do not explain all the variations in receptor number in hypertensive rats. Our results suggest a role of mineralocorticoids in the regulation of vascular AII receptors.
Hypertension
PMID:Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats. 631 55

To assess the hemodynamic changes during acute renal artery stenosis (RSt) and their dependence on alterations in the renin-angiotensin and sympathetic nervous systems, we studied conscious rats chronically instrumented with miniaturized pulsed-Doppler flow probes. Probes were implanted on the superior mesenteric and both renal arteries, and on the lower abdominal aorta for measurement of mesenteric (MR), renal (RR), and hindquarters (HQR) vascular resistance. Unilateral RSt, with a pneumatic cuff occluder that reduced flow by approximately 50%, increased mean arterial pressure (MAP) by 32%, reduced heart rate, and increased MR, nonstenotic (contralateral) RR and HQR. The hypertension was renin-dependent since plasma renin activity increased 6-fold and the angiotensin II (AII) antagonist, saralasin, significantly reduced MAP and regional resistances. The acute hypertension was also associated with increased neurogenic vasoconstrictor tone since hexamethonium markedly reduced MAP, MR, HQR and non-stenotic RR. Hexamethonium similarly decreased MAP during hypertension induced by AII infusion, whereas hypertension produced by the "pure" peripheral vasoconstrictor, phenylephrine, was unaffected by ganglionic blockade. In animals with peripheral sympathectomy produced by 6-hydroxydopamine, acute RSt produced hemodynamic changes similar in magnitude to intact animals; however, PRA increased 3-fold more than in intact rats. We conclude that hypertension induced by acute RSt in conscious rats is not only renin-dependent, but is also associated with inappropriately high neurogenic vasoconstrictor tone, presumably activated by indirect neural actions of AII.
Hypertension
PMID:Neural contribution to renal hypertension following acute renal artery stenosis in conscious rats. 633 57

A group of 13 male and 8 female out-patients (mean age: 40.57 years), with primary arterial hypertension, was submitted to two periods of treatment in a cross-over study with spironolactone and potassium canrenoate. Each preparation was given at the dose of 200 mg/day per os for 21 days, with a 10-day interval between treatments. Both preparations proved active on the systolic and diastolic pressure values controlled 7 days. However, potassium canrenoate showed a greater and more rapid effect, particularly on diastolic arterial pressure, as also demonstrated by the statistical analyses. PRA and aldosteronemia increased with both treatments, but this increase resulted significantly lower with potassium canrenoate. The minor stimulating action on the renin-angiotensin-aldosterone mechanism by potassium canrenoate may be the reason for its greater anti-hypertensive effect. Both treatments were perfectly tolerated locally and systemically.
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PMID:[Clinical study of the efficacy of oral potassium canrenoate and spironolactone in essential arterial hypertension]. 633 99


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