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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 the calcium entry blocker nitrendipine on blood pressure (BP) and renal hemodynamics were studied in rats with angiotensin II (ANG II)-induced hypertension. The ANG II was infused subcutaneously by implanted osmotic minipumps for 14 to 16 days. There was a progressive rise in BP in ANG II-infused rats to levels 58 mm Hg above basal by Day 10, whereas control rats with sham pumps remained normotensive. Nitrendipine or vehicle was administered by gavage to groups of control and hypertensive rats for 5 days, and clearance experiments were performed with the rats under anesthesia on the last day. The prolonged infusion of ANG II increased the renal vascular resistance and reduced the glomerular filtration rate and renal Na+ excretion. At a dose of 3 mg/100 g body weight, nitrendipine had no consistent effects on BP or renal function of control rats. By contrast, in rats with ANG II-induced hypertension, nitrendipine normalized both the BP and the changes in renal vascular resistance and glomerular filtration rate. Despite the fall in BP, nitrendipine caused a marked diuresis and natriuresis. Moreover, nitrendipine increased Na+ excretion of conscious, ANG II-hypertensive rats but not of controls. Thus, nitrendipine appears to be highly effective in reversing ANG II-induced hypertension and Na+ retention. These findings also indicate that the hypertension, renal vasoconstriction, and Na+ retention accompanying prolonged ANG II infusions may be mediated by calcium-dependent mechanisms.
Hypertension
PMID:Effects of a calcium entry blocker on blood pressure and renal function during angiotensin-induced hypertension. 315 2

The first adult case of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) deficiency is described. The impaired conversion of cortisol to cortisone (indicated by urinary cortisol and cortisone metabolites and failure to metabolize 11 alpha-[3H]cortisol to [3H]H2O), was associated with hypertension, hypokalemia, and suppression of the renin-angiotensin-aldosterone system. When established on a fixed Na+/K+ intake, dexamethasone, given orally, produced a natriuresis and potassium retention. Plasma renin activity became detectable. When hydrocortisone (10 mg daily s.c. for 4 d) was added, there was marked Na+ retention, a kaliuresis (urinary Na+/K+ falling from 1.2 to 0.15), with suppression of plasma renin activity and an increase in blood pressure. These changes were also seen with the subject on no treatment. Conversion of cortisone to cortisol was not affected. These results suggest that cortisol acts as a potent mineralocorticoid in 11 beta-OHSD deficiency. The major site for the oxidation of cortisol to cortisone is the kidney. In this patient congenital deficiency of 11 beta-OHSD results in high intrarenal cortisol levels which then act on renal type I mineralocorticoid receptors. This condition can be treated with dexamethasone, which suppresses cortisol secretion and binds to the type II glucocorticoid receptor. We suggest that 11 beta-OHSD exerts a critical paracrine role in determining the specificity of the type I receptor. In the normal state cortisol is converted by 11 beta-OHSD to cortisone which thus allows aldosterone to bind preferentially to the type I receptors in the kidney and gut. In this patient deficiency of 11 beta-OHSD results in high intrarenal cortisol concentrations that then bind to the type I receptor.
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PMID:Syndrome of apparent mineralocorticoid excess. A defect in the cortisol-cortisone shuttle. 316 27

The authors reviewed the effect of low dose dopamine administration (1-5 micrograms/kg/min) in neurosurgical patients with acute renal failure (5 cases) or hypernatremia (7 cases) in whom cerebral dehydration therapy for intracranial hypertension was thought to be causative of these disorders. Cases with hypernatremia (serum sodium over 155 mEq/l) were considered in the stage of impending acute renal failure as in the majority of cases serum creatinine levels were mildly elevated while urinary sodium was markedly diminished. Associated with systemic hypovolemia, in cases with acute renal failure (with serum creatinine over 3.5 mg/dl and urinary output of less than 20 ml/hr for more than 4 hour duration) the urinary sodium levels were less than 20 mEq/l. In all the cases treated by low dose dopamine, urinary output and sodium increased within 6 hours and in the following 24 hours stabilized urinary output with its elevated sodium (some 100 mEq/l) was obtained. As the result, elevated urea-nitrogen or serum sodium was rather easily washed out and the patients were kept adequately hydrated afterwards. Any complications such as aggravation of cerebral edema or convulsive disorder were not associated with this regime. The authors, therefore, would emphasize that low dose dopamine administration resulting in sodium diuresis and increase in renal blood flow is a practical way of method in treating patients with hypernatremia or acute renal failure caused by hyperosmolar agent infusion in their acute stage.
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PMID:[Renal protection in acute neurosurgical diseases--effect of a low dose dopamine with reference to acute renal failure and hypernatremia in patients with dehydration]. 322 69

There is conflicting evidence for the existence of a renal sodium excretory deficit in the salt-sensitive hypertensive Dahl S (DS) rat strain. While presentation of acute sodium loads, in vivo or in vitro, suggests that DS kidneys cannot excrete sodium as efficiently as kidneys from the salt insensitive genetic control Dahl R (DR) rat strain, metabolic studies of Dahl rats on a high-sodium diet are unable to differentiate between DS and DR rats. The natriuretic response to acute sodium loads is dependent on the integrity of structures in or near the anteroventral 3rd ventricle (AV3V) region. Therefore, it was thought that an AV3V-dependent chronic sodium challenge might also uncover an excretory defect in DS rats. We have investigated the renal response of inbred Dahl S (SS/Jr) and Dahl R (SR/Jr), and Sprague-Dawley rats to 48 h of dehydration; a manoeuvre which produces hyperosmolality and hypernatremia, with its renal response dependent on the integrity of the AV3V. Inbred Dahl S, Dahl R and Sprague-Dawley rats showed identical renal electrolyte excretory responses to both dehydration and rehydration. These results are discussed in terms of the mechanism of salt-induced hypertension and dehydration natriuresis.
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PMID:Dehydration natriuresis in Dahl S rats: no evidence for renal excretory deficit. 337 1

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.
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PMID:Long-term results of surgical and conservative treatment of patients with primary aldosteronism. 345 May 33

Sodium retention may partially offset the therapeutic action of some antihypertensive agents. To assess the effects of guanabenz on sodium balance, six men with mild to moderate hypertension were placed on diets with constant sodium intake (120 mEq/day) for approximately 4 weeks. After achieving sodium balance, the subjects received guanabenz (16-24 mg daily) for approximately 2 weeks. Mean supine blood pressure decreased from 144/93 to 133/86 mmHg during guanabenz treatment (p less than 0.001). Guanabenz therapy was associated with a decrease in body weight (mean +/- SE) from 85.4 +/- 7.0 to 84.4 +/- 6.8 kg (p less than 0.01). Sodium balance, glomerular filtration rate, plasma renin activity, mean maximal urine osmolality, fluid intake, urine volume, and serum sodium concentration were unchanged during guanabenz therapy. Three additional balance studies were performed during a period of greater sodium intake (180 mEq/day). Although higher doses of guanabenz were required to achieve blood pressure control, sodium balance still was not affected by the drug. Thus, an effective therapeutic dose of guanabenz administered for 2 weeks had no clinically significant effects on sodium or water homeostasis in patients with mild to moderate hypertension.
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PMID:Effects of guanabenz on sodium and water homeostasis. 345 82

The effects of chronic combined administration of angiotensin II, norepinephrine, aldosterone, and arginine vasopressin were compared with the response to each of these hormones administered alone. The studies were performed in dogs to determine the extent to which moderately inappropriate elevations of these hormones could enhance each other's ability to produce chronic hypertension and influence Na and water homeostasis. Blood pressure sensitivity to Na intake was also evaluated by infusing the hormones for 11 days at normal levels of Na intake followed by 11 days at high Na intake with ad libitum drinking. Combined hormone administration did not enhance each hormone's singular hypertensive actions. With aldosterone infusion alone and normal Na intake, mean arterial pressure rose nearly 15 mm Hg and an additional 3 mm Hg during high Na intake. Combined hormone infusion also resulted in a nearly 15 mm Hg rise during normal Na intake and an additional 3 mm Hg rise in mean arterial pressure during high Na intake. Marked Na retention and hypernatremia were observed with aldosterone infusion, while hyponatremia characterized arginine vasopressin infusion. The combined hormone infusion resulted in a tendency toward hypernatremia, although daily Na balance was not significantly changed. Daily water turnover was substantially increased and urine osmolality fell to hypoosmotic levels, despite elevated arginine vasopressin levels. Even with high Na intake, dogs receiving either angiotensin II, arginine vasopressin, or norepinephrine at the same concentrations showed 4 to 10 mm Hg increases in mean arterial pressure. Thus, humoral summation or synergism of these hormones probably does not play a major role in the development of chronic hypertension.
Hypertension 1986 Apr
PMID:Are hypertensive effects of aldosterone, angiotensin, vasopressin, and norepinephrine chronically additive? 351 49

Hypertension accompanying diabetes mellitus may involve abnormalities in at least two major blood pressure-regulating systems: the body sodium-fluid volume state and cardiovascular reactivity. In metabolically stable nonazotemic diabetes, exchangeable sodium is increased by 10% on average, regardless of age, insulin dependence or nondependence, or the presence or absence of diabetic retinopathy or clinical nephropathy (proteinuria greater than or equal to 0.3 g/24 hr). Possible contributing mechanisms include renal sodium retention and an extravascular shift of fluid and sodium; intracellular accumulation is not excluded. Circulatory volume is normal or low and the total exchangeable sodium/blood volume ratio increased. In hypertensive diabetes, the latter abnormality is particularly pronounced; systolic pressure tended to correlate with exchangeable sodium (r = 0.47, p less than 0.001) and diastolic pressure with the plasma sodium/potassium ratio (r = 0.25, p less than 0.05). Plasma aldosterone, renin, epinephrine, and norepinephrine levels are generally normal or sometimes low in metabolically stable nonazotemic diabetic patients with normal or high blood pressure; the plasma clearance of norepinephrine also appears to be unaltered. The cardiovascular pressor responsiveness to norepinephrine is often exaggerated relative to concomitant plasma concentrations, regardless of age, type of antidiabetic treatment, or presence or absence of diabetic retinopathy, peripheral neuropathy, or high blood pressure. Pressor responsiveness to angiotensin II also may sometimes be increased relative to plasma renin levels. Sodium retention and diabetic vasculopathy of resistance vessels could be important complementary mechanisms of hyperreactivity. In diabetes with mild hypertension, diuretic treatment restored exchangeable sodium, norepinephrine pressor responsiveness, and blood pressure toward normal. Thus sodium retention and cardiovascular hyperreactivity tend to occur even at the normotensive, nonazotemic stage of diabetes and may concomitantly predispose for the frequent development of hypertension in the diabetic population.
Hypertension
PMID:Pressor factors and responsiveness in hypertension accompanying diabetes mellitus. 390 20

The anteroventral third ventricle (AV3V) region plays an important role in fluid and electrolyte balance and cardiovascular control in the rat; however, experiments in other species have raised questions about the universality of findings in the rat. The effects of discrete lesions placed within the AV3V area on hydromineral balance, the pressor response to angiotensin II given intravenously, and the initiation of a renin-dependent model of hypertension were examined in the dog. A transpharyngeal approach to the optic chiasm enabled us to destroy only the anterior aspects of the AV3V region (aAV3V group) or to include the entire nucleus medianus (NM) as well (aAV3V + NM group). Lesions of the aAV3V caused polydipsia and transient hypernatremia and hyperosmolality. In contrast, adipsia and a sustained increase in plasma sodium levels and osmolality were observed in dogs with lesions of the aAV3V plus the entire NM. Neither lesion altered baseline arterial pressure, heart rate, plasma levels of catecholamines and vasopressin, or total plasma protein levels. Only in aAV3V + NM lesioned dogs was there a tendency for plasma angiotensin II immunoreactivity to be elevated above control values at 2 and 4 days after operation. Neither lesion attenuated the pressor response to intravenous angiotension II or the initiation of renal hypertension induced by aortic coarctation. As observed in other species, structures within the AV3V region participate in hydromineral balance in the dog; however, in the dog portions of the NM dorsal to the AV3V region are essential for the mediation of drinking behavior.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:The anteroventral third ventricle region. Participation in the regulation of blood pressure in conscious dogs. 399 35

There have been numerous accounts of women on ovulation inhibitors developing hypertension or reactifying or intensifying previous hypertension. Concerning frequency of significant hypertension in pill users, there are reports varying from .66% (or even 0%) to 19%. The time interval between start of medication and manifestation of hypertension also varies according to different sources from 7 days to 5 years, with the critical point usually around 6-8 weeks. Degree of hypertension after ovulation inhibitors ranges from mildly significant increases in systolic and/or diastolic blood pressure to malignant hypertension with irreversible kidney insufficiency. Early observable symptoms of hypertension include migrainelike headaches and rapid weight gain (sodium and water retention). After discontinuation of the medication, normal blood pressure is attained either within a few days or after 6-8 months. If normalization of blood pressure does not occur spontaneously there may be other causes (e.g., secondary vascular disorders). Concerning pathogenesis of ovulation-inhibitor-related hypertension, changes (increases) in the renin-angiotensin-aldosterone system are assumed to play a major role (almost all women on the pill exhibit elevated renin-angiotensin-aldosterone activity). Sodium retention may also be determinative. Many clinical and laboratory studies have demonstrated that it is the estrogen content of ovulation inhibitors that is responsible for the increased plasma renin activity. The study recommends: 1) women who wish oral contraceptive therapy should give careful family and personal histories and be tested for blood pressure before and during treatment (monthly, then after 6 months twice yearly); 2) careful supervision is indicated for women with high blood pressure or other cardiovascular disorders in their history, present or former kidney disorders, arterial hypertension, pregnancy toxemias, adipositas, or diabetes mellitus; 3) abnormal weight gain may be an early symptom; 4) if any rise in blood pressure is observed, ovulation inhibitor medication should be discontinued immediately; and 5) ovulation inhibitor-induced hypertension should be considered in differential diagnosis in young women with arterial hypertension.
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PMID:[Oral contraceptives and arterial hypertension]. 437 45


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