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

In 14 patients with arterial hypertension secondary to chronic renal parenchymal disease and impaired renal function, 24-h ambulatory and casual blood pressure readings plasma, angiotensin II, aldosterone, arginine vasopressin and atrial natriuretic peptide, creatinine clearance, plasma lipids and lipoproteins, and body weight were determined after consecutive 3-week periods on placebo and sustained release verapamil 240 mg/day. Verapamil reduced the mean 24-h ambulatory blood pressure from 152/104 to 142/97 mm Hg. Blood pressure was significantly reduced during the daytime and the evening, but not at night. Casual blood pressure was also significantly reduced from 176/106 mm Hg to 154/96 mm Hg. No significant changes were found in the hormones, creatinine clearance, plasma lipids and lipoproteins, heart rate or body weight. The atrial natriuretic peptide level was significantly correlated with the calculated creatinine clearance (r = -0.797). Thus, sustained release verapamil 240 mg as a single daily dose had a moderate hypotensive effect in patients with chronic renal disease without inducing tachycardia, activation of the renin-angiotensin-aldosterone system, or increasing body weight, and without altering renal function and plasma lipids and lipoproteins. The negative correlation between atrial natriuretic peptide and glomerular filtration rate supports the hypothesis that the extracellular volume increases during progression of renal disease.
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PMID:Sustained release verapamil in renal hypertension. 296 36

Atrial natriuretic peptide (ANP) and arginine vasopressin concentrations were measured in 9 patients with pregnancy-induced hypertension. The results were compared to those found in 7 normal pregnant women matched for age, duration of pregnancy, and parity. Plasma ANP levels were significantly higher in the pregnancy-induced hypertension patients than in the control group. Plasma arginine vasopressin concentrations, however, were not significantly different in the two populations. The mechanism of the observed rise in ANP concentrations in the patients with pregnancy-induced hypertension is not known. However, it may be related to a rise in intra-atrial pressures secondary to hypertension, an increase in baroreceptor discharge as a result of hypertension, or, less likely, the ANP may be released from extracardiac sites.
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PMID:Atrial natriuretic peptide and arginine vasopressin in pregnancy and pregnancy-induced hypertension. 296 20

Our previous studies have demonstrated: 1) that i.v. quinpirole (LY171555), a selective dopamine D2 receptor agonist, has a dose-dependent pressor effect in conscious rats which is mediated by activation of sympathetic outflow and vasopressinergic activity, and 2) that the activity of central dopaminergic neurons is reduced in deoxycorticosterone acetate (DOCA)/NaCl hypertensive rats. To elucidate the role of central and peripheral dopaminergic systems in the pathogenesis of DOCA/NaCl hypertension, we examined the effects of quinpirole on mean arterial pressure, heart rate, plasma norepinephrine, epinephrine, arginine vasopressin and atrial natriuretic peptide (ANP) in conscious 4-week-old DOCA/NaCl hypertensive and normotensive control rats. Quinpirole (1 mg/kg i.v.) increased mean arterial pressure in both groups, but the pressor response was attenuated in DOCA/NaCl rats. Paradoxically, quinpirole-induced increments in plasma norepinephrine, epinephrine and arginine vasopressin were greater in DOCA/NaCl rats. In addition, quinpirole induced a 2-fold increase in plasma ANP (P less than .01) in both DOCA/NaCl and control rats. Pretreatment with domperidone (2.5 mg/kg i.v.), a peripherally acting dopamine D2 antagonist, enhanced the maximum pressor response to quinpirole in both groups, restored the quinpirole-induced pressor response to control levels in the DOCA/NaCl rats and blocked the stimulatory effect of quinpirole on ANP release in both groups. These data indicate that peripheral dopamine D2 receptors modulate ANP secretion in the rat. The observation that the quinpirole-induced increment in plasma ANP was enhanced in DOCA/NaCl rats supports the hypothesis that the blunted pressor response to quinpirole in this model is related to enhanced ANP release.
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PMID:Blunted pressor responsiveness to quinpirole, a specific dopamine D2 receptor agonist, in conscious deoxycorticosterone acetate/NaCl hypertensive rats is related to atrial natriuretic peptide release. 296 76

The specific vasopressin receptor of V1 vascular subtype, which mediates platelet aggregation, has been found on human platelets. We investigated the binding characteristics using tritiated arginine vasopressin [3H]-AVP and platelet aggregation with AVP turbidometrically in normal subjects, patients with WHO class II essential hypertension and patients with malignant-phase hypertension. In essential hypertensives Bmax was significantly higher than that in normal subjects, but there were no differences in affinity and the maximal percentage aggregation between them. In malignant-phase hypertensives Bmax and maximal percentage aggregation were significantly lower than those in normals and essential hypertensives, although there was no difference in the affinity between them. With radio-immunoassay, the mean platelet-free plasma AVP level was significantly higher in malignant-phase hypertensives than those in normals and essential hypertensives, whereas there was no difference in mean platelet AVP levels between them. In essential hypertensives Bmax and maximal percentage aggregation did not change, but in malignant-phase hypertensives Bmax increased significantly and maximal percentage aggregation tended to normalize after treatment.
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PMID:Platelet vasopressin receptor in essential hypertension. 297 78

The relationship of arginine vasopressin (AVP) in plasma to cyclic adenosine 3' 5'-monophosphate (cAMP), sodium excretion in urine, and arterial blood pressure were determined during intravenous infusion of hypertonic sodium chloride solution (500 ml of 50 g/l) in 10 normotensive control subjects and in 11 normotensive and 10 hypertensive patients with chronic glomerulonephritis and relatively well preserved kidney function. The concentration of AVP in plasma increased 2-4 fold, osmolality in serum increased 12-16 mosmol/kg, and urinary excretion of cAMP increased 20-40% during sodium loading to the same extent in all three groups. Sodium and water excretion were higher during the sodium loading in the hypertensive patients, but not in the normotensive patients when compared to the control subjects. Neither AVP nor changes in AVP correlated significantly with changes in cAMP excretion, sodium excretion or blood pressure. In the control subjects the level of parathyroid hormone in serum was unchanged during the sodium chloride infusion. Water loading without sodium loading in eight of the control subjects caused a decrease in the excretion of cAMP. In conclusion, the increase in cAMP excretion in urine during the sodium loading might be explained by an AVP-induced stimulation of renal cAMP production. The study does not suggest that AVP plays a role in the increased sodium excretion during sodium loading or in the development of hypertension or chronic glomerulonephritis.
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PMID:Arginine vasopressin and cyclic adenosine monophosphate during acute sodium loading in chronic glomerulonephritis. 298 6

The effects of exogenous corticotropin releasing factor and arginine vasopressin were evaluated in 6- and 11-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Basal adrenocorticotropic hormone (ACTH) and vasopressin levels did not differ between SHR and WKY, but basal corticosterone level was higher in 6-week-old SHR (p less than 0.01). To block endogenous corticotropin releasing factor secretion and nonspecific systemic responses, both groups were pretreated with chlorpromazine, morphine, and sodium pentobarbital anesthesia before measurement of ACTH responses to corticotropin releasing factor and vasopressin infusion. Basal ACTH level was lower in anesthetized 6-week-old SHR than in age-matched WKY (p less than 0.01), but no difference was seen between 11-week-old WKY and SHR. The ACTH response to corticotropin releasing factor in 6-week-old WKY was significantly greater than that in age-matched SHR (p less than 0.01), whereas in 11-week-old SHR and WKY the response was similar. Compared with responses in WKY, SHR showed an increased ACTH response to high doses of vasopressin (0.25 micrograms/100 g body weight) at both ages (p less than 0.05). These results indicate that the ACTH response to corticotropin releasing factor is blunted in the early stages of hypertension in SHR but later recovers. These abnormal responses to corticotropin releasing factor and vasopressin may be related to the development of spontaneous hypertension.
Hypertension 1986 May
PMID:Adrenocorticotropin responses to corticotropin releasing factor and vasopressin in spontaneously hypertensive rats. 300 24

Although abnormalities in the vasopressin system have been reported in spontaneously hypertensive rats (SHR), neither short-term nor long-term administration of the vasopressin antagonist d(CH2)5-Tyr(Me)arginine vasopressin (AVP), which selectively blocks the action of vasopressin on vascular (V1) receptors, altered the course of hypertension in SHR. In the current study, long-term administration of a different vasopressin antagonist, d(CH2)5-D-Tyr(Me)VAVP, to SHR and Wistar-Kyoto rats (WKY) from 4 to 12 weeks of age significantly attenuated the development of systolic hypertension in SHR (p less than 0.05) without altering blood pressure in normotensive WKY. The antagonist was delivered subcutaneously by osmopump at 0.1 microgram/hr. Systolic blood pressure was monitored twice weekly by tail plethysmography beginning at 5 weeks of age. In a second group of SHR, the drug infusion was continued until 18 weeks of age. In this group, the attenuation of systolic hypertension by the drug was extended and became more prominent (p less than 0.007). Resting mean arterial pressure measured by indwelling catheters in the conscious state at 18 weeks of age was significantly reduced in the antagonist-treated SHR (144 +/- 4 vs 157 +/- 4 mm Hg; p less than 0.05). Heart rate also was significantly reduced by the drug (351 +/- 6 vs 392 +/- 7 beats/min; p less than 0.001). Following measurement of mean arterial pressure in the rats at 18 weeks of age, the osmopumps were removed and systolic blood pressure, mean arterial pressure, and heart rate were observed until 22 weeks of age.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Nov
PMID:Attenuation of spontaneous hypertension in rats by a vasopressin antagonist. 305 58

The vasoconstrictor actions of arginine vasopressin (AVP) have been shown to occur in concentrations much lower than previously thought. Pressor responses to AVP are a poor index of vasoconstrictor activity since, in contrast to other vasoconstrictor agents, the expected rise of pressure is offset by dose-dependent decreases of cardiac output. The mechanisms for this appear to be, in large part, modulation of the autonomic nervous system whereby AVP enhances vagal nerve activity and reduces peripheral sympathetic nerve activity. AVP enhancement of baroreceptor reflex gain is in part responsible for these changes in some species (dog and rabbit), but not in others (rat). The release of AVP appears to contribute significantly to the normalization of arterial pressure in volume-depleted and hypotensive states. The link between plasma AVP and hypertension remains unclear, but it appears likely that it has an important permissive action in the development of sodium-dependent forms of hypertension.
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PMID:Vasopressin and blood pressure regulation. 306 Feb 96

Blood volume, extracellular volume, blood pressure and the plasma levels of angiotensin II, aldosterone, adrenaline, noradrenaline and arginine vasopressin were determined in sixteen normotensive (group 1) and thirteen hypertensive patients (group 2) with chronic glomerulonephritis and in eleven normotensive control subjects (group 3). Blood volume and extracellular volume did not differ between the groups and no significant differences were found in any of the hormones measured when comparing group 1 or group 2 with group 3. In the hypertensives but not in the normotensives or control subjects, a highly significant positive correlation was found between diastolic blood pressure and blood volume (rho = 0.75, P less than 0.01) and between diastolic blood pressure and extracellular volume (rho = 0.74, P less than 0.01). Blood volume and extracellular volume correlated (P less than 0.05) in each of the groups. In conclusion, although no expansion of either blood or extracellular volume was found in chronic glomerulonephritis, a positive volume-pressure relationship could be demonstrated in hypertensive patients suggesting a role of volume factors in the pathogenesis in early stage chronic glomerulonephritis. The study does not give support to a major role of either angiotensin II, arginine vasopressin or catecholamines in the maintenance of nonmalignant hypertension in early stage chronic glomerulonephritis.
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PMID:Relationship of angiotensin II, aldosterone, arginine vasopressin, adrenaline and noradrenaline in plasma, blood and extracellular volumes to blood pressure in chronic glomerulonephritis. 308 77

Electrolytic lesions of the A1 noradrenaline cells in the caudal ventrolateral medulla cause transient hypertension and bradycardia in the conscious rat, as previously described in the rabbit. The lesions produced 100-fold increases in plasma arginine vasopressin, 40-fold increases in plasma adrenaline and fourfold increases in plasma noradrenaline levels. Absence of circulating vasopressin [homozygous diabetes insipidus rats (DI)] or circulating adrenaline (adrenalectomized rats) did not affect A1 hypertension, but sympathectomy with systemic 6-hydroxydopamine (6-OHDA) significantly attenuated A1 hypertension. A factorial experiment was performed to assess the relative contributions of these three peripheral effector mechanisms in a quantitative manner, with combined deficiencies of any two or of all three of these effector systems. Results suggest A1 hypertension in the rat to be primarily mediated through increased sympatho-adrenal activity. The largest component of hypertension (66%) results from increased sympathetic vasoconstrictor nerve activity, and a smaller part (34%) reflects the action of circulating adrenaline. Increases in vasopressin levels do not contribute to A1 hypertension, although vasopressin makes a major contribution to A1 lesion bradycardia.
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PMID:Relative importance of sympathetic nerves and of circulating adrenaline and vasopressin in mediating hypertension after lesions of the caudal ventrolateral medulla in the rat. 309 Jan 38


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