UMLS:C0020538 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

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

In order to investigate the vasopressor role of ADH in the regulation of blood pressure, passive immunization experiments with an antibody to AVP were carried out in experimentally hypertensive rats. In hypertensive rats treated with deoxycorticosterone acetate (DOCA), spontaneously hypertensive rats (SHR) and spontaneously hypertensive stroke-prone rats (SHR-sp), the intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood pressure of 11 approximately 25mmHg, while in rats with two-kidney Goldblatt hypertension and normal rats, the blood pressure was not affected. This strongly suggests that ADH contributed to systemic vaso-constriction in DOCA hypertension and spontaneous hypertension in rats.
...
PMID:[The vasopressor role of ADH in the maintenance of blood pressure in experimentally hypertensive rats (author's transl)]. 49 16

A variety of experimental approaches have shown that AVP and mineralocorticoids stimulate Na+ transport through their effects on the number and kinetic properties of amiloride-sensitive Na+ channels in the apical membrane. The different mechanisms by which AVP and mineralocorticoid act on the Na+ channel provide a basis for synergism in their actions, perhaps by a scheme such as that proposed in Figure 5. However, the details of this interaction will require a better understanding of the molecular details involved in activating quiescent channels, increasing their open probability, and reorientating or inserting channels to an operational position in the apical membrane. Electrophysiological and biochemical approaches have gone a long way toward elucidating some of these molecular details. But the latter approach in particular has indicated that the Na+ channel may have multiple regulatory subunits and thus be a target for several intracellular second messengers and autacoids other than those involved in the actions of AVP and aldosterone. The challenges for future research in this area are multiple. It seems likely that the primary amino acid sequence of the channel subunits will soon become available from cloning and sequencing approaches, but the application of this knowledge to understanding how the subunits are integrated into the complete protein and mediate regulatory signals will be a formidable task. It will be important to determine the normal extracellular signals (other than aldosterone and AVP) and the associated intracellular second messengers that alter channel activity. It will also be important to understand how some species such as the rabbit may "turn off" the stimulatory effect of AVP on Na+ reabsorption in the CCD, and how this regulatory process is altered when these cells are cultured. At the whole animal level, it will also be important to investigate whether changes in one or more of the normal regulatory pathways that impinge on the Na+ channel might be involved in a diminished ability to excrete a salt load, as is observed in some models of hypertension. All of these issues need to be understood at the molecular level, and it seems likely they will provide exciting physiological insights at all levels.
...
PMID:Regulation of Na+ channels in the cortical collecting duct by AVP and mineralocorticoids. 131 21

The hemodynamic responses and the role of renal nerves in the physiopathogenesis of acute (45 min) aortic coarctation hypertension were studied in conscious rats. The hemodynamic responses elicited by aortic constriction in intact and bilaterally nephrectomized rats were analyzed by means of miniaturized pulsed-Doppler flow probes. Anephric rats presented a smaller increase in mean carotid pressure (MCP) and calculated aortic resistance during aortic coarctation than did intact animals. Reflex bradycardia throughout the experiment did not differ significantly between the two groups. The pressor response following aortic coarctation in untreated renal-denervated rats was similar to that found in intact subjects. Renal-denervated rats previously treated with V1-vascular arginine vasopressin antagonist [d(CH2)5Tyr(Me)AVP] showed the same hypertensive response as control renal-denervated rats. Previous treatment of renal-denervated rats with saralasin (an angiotensin II antagonist) produced a significant reduction in the hypertensive response throughout the experiment when compared to untreated renal-denervated rats. Similarly, rats treated with the vasopressin antagonist plus saralasin showed a blunted hypertensive response following aortic coarctation. The results for rats previously treated with vasopressin antagonist plus saralasin did not differ from those obtained with saralasin alone. Overall, the results of aortic coarctation hypertension obtained in the present study indicate that: 1) Anephric rats showed a blunted hypertensive response due to the lack of neuro-humoral release of vasopressor substances (e.g. angiotensin II and vasopressin) triggered by the kidneys, when only the mechanical factor of constriction was present; 2) The lack of afferent feedback from the kidneys in renal-denervated rats for vasopressin release from the central nervous system allowed angiotensin II to play the major physiopathological role associated with the mechanical factor in the hypertensive response.
...
PMID:Mechanical and neuro-humoral factors in acute aortic coarctation hypertension. 160 37

The contribution of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure was investigated in high sodium-fed rats 4 weeks after the induction of one-kidney, figure-8 renal wrap hypertension. Arterial pressure was significantly greater in renal-wrapped rats than in sham-operated animals. The contribution of the sympathetic nervous system was assessed functionally by measuring the arterial pressure response to ganglionic blockade and estimating the apparent rate of release of norepinephrine. The contribution of vasopressin was assessed by administration of the vascular antagonist d(CH2)5Tyr(Me)-AVP. Whole-animal vascular responsiveness and cardiac baroreceptor reflex sensitivity were determined by graded intravenous bolus injections of angiotensin II, vasopressin, and phenylephrine. Hypertensive rats demonstrated an exaggerated reduction in arterial pressure to autonomic blockade before and after blockade of vascular vasopressin receptors. There was a significant 27% increase in the apparent rate of release of norepinephrine into the plasma. Administration of d(CH2)5Tyr(Me)-AVP did not affect arterial pressure when given alone. However, after ganglionic blockade, inhibition of the vasopressin system elicited similar falls in blood pressure in both normotensive and hypertensive rats. Arterial pressure dose-response effects of phenylephrine, angiotensin II, and vasopressin were similar between renal-wrapped and sham-operated animals; however, cardiac baroreceptor reflex sensitivity was suppressed in the hypertensive rats. These studies indicate that the maintenance of arterial pressure in chronic, high sodium renal-wrap hypertension is associated with an augmented sympathetic nervous system function.
Hypertension 1992 Jul
PMID:Sympathetic nervous system in high sodium one-kidney, figure-8 renal hypertension. 161 57

Studies were performed to characterize the regulation of central vasopressin (AVP) receptors in deoxycorticosterone acetate (DOCA)-NaCl-treated and control rats, and in DOCA-treated primary neuronal enriched cell cultures. Uninephrectomized rats were given NaCl to drink and implanted subcutaneously with a silastic implant containing 200 mg/kg DOCA. [3H]AVP binding to a diencephalic block of tissue was examined. Whereas DOCA-NaCl treatment did not affect the affinity of [3H]AVP binding, the total number of AVP receptors was increased between 3 and 14 days following DOCA-NaCl administration. No differences in the number of binding sites were present in the established (35-56 days after DOCA-NaCl administration) stages of hypertension. To determine whether the increase in [3H]AVP binding was a direct effect of DOCA on neurons or related to the hormonal, volume or other physiologic changes that DOCA-NaCl treatment causes in the whole animal, [3H]AVP binding was examined in neurons grown in culture that was treated with DOCA. Scatchard analysis demonstrated that DOCA treatment (compared to control) produced an increase in the number but no change in the affinity of the AVP binding sites in primary neuron-enriched cultures. Treatment of cultured neurons with other steroids (estrogen, corticosterone, or aldosterone), did not change the kinetics of [3H]AVP binding, suggesting that the effects of DOCA on the AVP receptor were specific for this steroid. These data indicate that, in comparison to control rats, DOCA-NaCl hypertensive rats, have an enhanced number of AVP receptors in the diencephalon, perhaps as a direct result of an interaction between DOCA and AVP receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Central vasopressin receptors are upregulated by deoxycorticosterone acetate. 183 96

The aim of the present study was to compare effects of intravenous infusion of vasopressin AVP and V1 receptors blockade on blood pressure and heart rate in normotensive (WKY) and spontaneously hypertensive (SHR) rats. A 20 min vasopressin infusion (1.2 ng/kg/min) elicited significantly greater increase in mean blood pressure (MP) in SHR than in WKY. Heart rate was significantly reduced in SHR while nonsignificantly in WKY. A 20 min dEt2 AVP (V1 antagonist) infusion (0.5 microgram/kg/min) elicited significant decrease in MP and increase in heart rate (HR) in SHR, but produced no effect in WKY. The data indicate that SHR are more susceptible to pressor and hypotensive effects of sustained elevation of AVP and AVP antagonist. The results support the hypothesis that AVP may contribute to pathogenesis of hypertension.
...
PMID:Effects of vasopressin and V1 receptors blockade on blood pressure and heart rate in spontaneously hypertensive rats. 184 Mar 31

Male Sprague-Dawley rats were uninephrectomized and given either deoxycorticosterone (DOC) pivalate (12.5 mg three times weekly) and 1% NaCl/0.2% KCl to drink for 4 weeks (DOC-treated), after which DOC was stopped and tap water substituted (post-DOC), or tap water to drink throughout (controls), DOC treatment increased blood pressure, serum sodium, plasma atrial natriuretic peptide (P-ANP) and plasma deoxycorticosterone (P-DOC) (P less than 0.05), while serum potassium, plasma renin and plasma angiotensin II were lower (P less than 0.05) than in control animals. Plasma vasopressin (P-AVP) was also raised but not significantly. These changes persisted for up to 4 weeks post-DOC and, in the case of plasma renin, plasma angiotensin II, P-AVP and P-ANP, for up to 12 weeks. Total body sodium was also increased at 2 weeks post-DOC (P less than 0.05). Rats which were adrenalectomized after 4 weeks of DOC treatment in which DOC injections were stopped, then drank either NaCl/KCl or tap water; blood pressure and P-DOC remained elevated while plasma renin remained suppressed. There were more deaths in rats given NaCl/KCl (five of six) than in the group given water (one of six). Rats treated with a subcutaneous DOC silastic implant had a comparable rise in blood pressure to rats given DOC injections. However, after removal of the implant, while blood pressure remained elevated, P-DOC levels were not raised and plasma renin rose to control levels after 4 weeks. These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC.
...
PMID:Hormone and electrolyte changes in post-deoxycorticosterone salt hypertension in rats. 196 84

Experiments were performed to test the hypothesis that Na retention and Na in the diet are not required to initiate central aldosterone induced hypertension. Rats were fed either standard rat chow or Na-deficient diet and infused intracerebroventricularly (i.c.v.) with aldosterone (28 ng/h) dissolved in artificial cerebrospinal fluid (vehicle) or vehicle alone. In Na-replete rats the central infusion of aldosterone did not promote Na or water retention, prior to increases in systolic blood pressure (SBP). Infusion of aldosterone in Na-deficient rats also initiated a rise in SBP, although the response was delayed. In neither group of rats did aldosterone infusion significantly change plasma Na, K, renin, norepinephrine (NE) or vasopressin (AVP) concentrations. There was no significant increase in plasma aldosterone concentration in Na replete rats centrally infused with aldosterone. Infusion of vehicle had no effect on SBP. We conclude that central aldosterone infusion initiates an increase in blood pressure by a mechanism independent of Na retention. Furthermore, increased concentrations of systemic renin, vasopressin, and activation of the sympathetic nervous system do not appear to be involved in maintaining hypertension.
...
PMID:Central infusion of aldosterone increases blood pressure by mechanisms independent of Na retention. 219 23

Three groups of dogs were studied to determine to what extent the suppression of plasma renin activity (PRA), natriuresis, and hyponatremia, seen with chronic elevations of plasma vasopressin (AVP), were caused by volume expansion or some other more direct actions of AVP. The dogs of group 1 (n = 7) were infused with AVP (0.36 ng/kg/min, i.v.) for 2 weeks, while water intake was maintained at a constant level. The dogs of group 2 (n = 6) were permitted to drink ad libitum during AVP infusion. The dogs of group 3 (n = 7) were infused with AVP while total body weight and volume were maintained at a constant level by use of an electronically servocontrolled water infusion system. Group 1, with fixed water intake, retained a large fluid volume (1.4 L), with an associated 36 mm Hg rise in mean arterial blood pressure (MAP). Associated with this hypertension and increased volume were a suppression of PRA and substantial decreases in plasma sodium concentration with increased excretion of sodium. With ad libitum drinking (group 2), only mild volume expansion occurred, with no significant elevations of MAP or changes in sodium excretion. With a volume expansion of 300-400 ml, there was a significant decrease of PRA and plasma sodium concentration. Group 3, servocontrolled dogs, exhibited no change in MAP, plasma sodium concentration, or PRA throughout the 2-week period of AVP infusion. Sodium excretion was mildly elevated only on the first day of AVP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Vasopressin excess: relative contribution of volume retention versus direct actions on renin secretion and sodium excretion. 243 76

To understand the regulation of vasopressin (AVP) receptors in spontaneous hypertension, we investigated the pressor response of AVP in the perfused mesenteric vasculature, AVP binding sites in the membrane preparation of the same vascular bed, and the production of inositol trisphosphate (InsP3) stimulated by AVP in the aorta of spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), and Wistar rats (WR) at different ages (4-16 weeks). Plasma AVP concentrations were similar in SHR, WKY, and WR at all ages. The density of AVP vascular binding sites was significantly higher in WKY than in SHR and WR at 12 weeks. Receptor affinity was similar in all strains. The pressor response of the mesenteric vasculature to AVP was similar in the three strains of rats at 4 weeks (prehypertensive stage) and increased progressively in SHR compared with WKY and WR at 8 and 12 weeks of age by 43 and 35%, respectively, and by more than 80% at 16 weeks of age (established hypertensive stage). There was no difference in vascular sensitivity to AVP. A significantly increased pressor response to a supramaximal dose of norepinephrine was also found at 16 weeks in SHR, but not in younger rats. InsP3 production in the aorta in response to AVP was increased in SHR at 8, 12, and 16 weeks, compared with WKY and WR. These results suggest that the vascular response to AVP is increased in SHR, in spite of decreased or normal density of binding sites compared with WKY or WR.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Vasopressin receptors and inositol trisphosphate production in blood vessels of spontaneously hypertensive rats. 252 49

1 2 3 4 5 6 7 8 9 10 Next >>