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

Studies of the mechanism of ACTH induced hypertension in sheep have led to the hypothesis that adrenocortical steroids may raise blood pressure by a "hypertensinogenic" action which can be distinguished from effects mediated by occupancy of classical mineralocorticoid or glucocorticoid receptors. This concept is supported by recent structure-activity studies using synthetic and naturally occurring steroids. Development of steroid hypertension is rapid (4-6 h) and although associated with an increase in cardiac output, changes in total peripheral resistance are important. Many different mechanisms have been proposed to explain how steroids raise blood pressure. In sheep it has been shown that the autonomic nervous system and vasoactive prostanoids appear to buffer, rather than cause, the rise in blood pressure. The renin-angiotensin system, AVP and serotonin are also unlikely to be involved. Further, the effects of steroids on blood pressure are not simply related to effects on Na status and changes in body fluid volumes. A direct involvement of the central nervous system remains to be established. In understanding how ACTH raises blood pressure, studies in sheep have shown that it is important to try and dissociate the effects of steroids involved in development of hypertension from the many other actions of steroids.
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PMID:Understanding the mechanism of adrenocortical steroid hypertension. 253 48

The role of vasopressin (AVP) and angiotensin II (ANG II) in the onset of acute (45 min) aortic coarctation hypertension was studied in conscious rats. Changes in mean carotid pressure (MCP) and heart rate (HR) were measured in four groups of rats. Control rats presented a hypertensive response that attained a plateau 5 min after coarctation and remained near this level throughout the experiment. Rats treated with AVP V1-vascular receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5Tyr(Me)AVP] presented a prompt rise in MCP similar to the control rats, but in contrast to this group, the MCP started to decline progressively. Rats treated with saralasin presented a delay in the onset of hypertension right after coarctation but slowly attained values similar to those for control rats. In contrast, the rats treated with AVP antagonist plus saralasin showed a blunted MCP elevation throughout the experiment. Reflex bradycardia observed in the rats treated with saralasin or the AVP antagonist plus saralasin was similar to that observed in the control rats, whereas for the group treated only with AVP antagonist, the reflex bradycardia was more intense than for the other three groups, indicating an increased sensitivity of the baroreflex. These data demonstrate that in addition to the mechanical effect of aortic constriction, both ANG II and AVP participate in the onset of acute aortic coarctation hypertension. Moreover, the results indicate that ANG II acts on the prompt (5 min) rise in pressure, whereas AVP is responsible for the maintenance (30-45 min) of the arterial pressure elevation.
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PMID:Acute aortic coarctation hypertension: role of vasopressin and angiotensin II. 258 3

It has been demonstrated that an increase in dietary calcium intake can lower the blood pressure of the hypertensives. We examined the effect of dietary calcium on blood pressure and vascular reactivity in DOCA-salt hypertensive rats. Blood pressure was significantly decreased after four weeks of calcium feeding. Nevertheless, the development of hypertension was not completely avoided. There was no difference between the calcium fed group and the control group in their response to NE, KCl and AVP in tail artery helical strips in normal calcium medium in vitro. However, the responses of these two groups to NE (10(-6) M) and AVP (10mU) were significantly different in Ca2+-free medium. Furthermore, the tail artery from Ca-fed group was less responsive to K+-induced relaxation. Since K+-induced relaxation has been applied to indicate the activity of Na+-K+ pump, we suggest that the activity of Na+-K+ pump may be involved and that the change in vascular reactivity to agonists might be rather insignificant in lowering the blood pressure of Ca-fed DOCA-salt hypertensive rats.
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PMID:Effect of calcium diet on the vascular reactivity of DOCA-salt hypertensive rats. 274 86

The development of blood pressure was monitored by the tail-cuff method in normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) receiving ethanol (alcohol) in drinking water from weaning (approximately 1 month of age). Alcohol administration over a 3-month period attenuated the development of hypertension in SHRSP and also caused a small reduction of the initial blood pressure rise in WKY. This was accompanied by a reduction of fluid intake and an increase of circulating antidiuretic hormone (arginine vasopressin; AVP). Circulatory volume remained constant. Direct measurement of arterial blood pressure in conscious rats before and after autonomic blockade confirmed the antihypertensive effect of alcohol in SHRSP and indicated that it is at least partly dependent on altered activity of neural mechanisms. Sudden withdrawal of alcohol caused an immediate increase of fluid intake followed by a rise of blood pressure lasting several days in both WKY and SHRSP. This withdrawal hypertension could not be attributed to changes in plasma catecholamines or AVP.
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PMID:Effects of chronic alcohol consumption and alcohol withdrawal on blood pressure in stroke-prone spontaneously hypertensive rats. 276 25

1. Hereditary hypothalamic diabetes insipidus was introduced into the New Zealand genetically hypertensive (NZGH) rat and its normotensive substrain (NZN) by cross-breeding males with female Brattleboro diabetes insipidus (DI) rats. 2. Selective breeding of the resultant DI/hypertensive (DI/H) rats on the basis of maximum systolic blood pressure and vasopressin deficiency produced animals in the F6 generation with blood pressures at 10 weeks of age higher than in DI/normotensive rats (DI/N), but much lower than in age-matched NZGH animals. Age-matched NZN and DI/N rats had comparable blood pressures. 3. Fluid turnover was far greater in DI/N and DI/H rats than in NZN and NZGH rats. Although comparable in DI/N and NZN rats, water balance (intake-urinary loss) was reduced in DI/H rats by comparison with NZGH rats. 4. Sodium balance was lower in DI/N rats compared with NZN rats but did not differ between DI/H and NZGH animals. Both DI groups had lower potassium balances. 5. Basal plasma vasopressin was elevated in NZGH rats compared with NZN rats, while vasopressin was undetectable in DI animals. Plasma aldosterone levels did not differ between groups, but corticosterone was lower in DI/N and DI/H rats by comparison with NZN and NZGH rats. 6. Replacement of vasopressin to achieve physiological plasma hormone levels restored normal fluid management in DI animals and was associated with a modest increase in systolic blood pressure in DI/N animals, compared with sham-treated rats. A much larger increase in blood pressure was observed in AVP-treated DI/H animals, but blood pressure remained below that in NZGH rats. 7. It is apparent that vasopressin may contribute to the hypertension of the NZGH rat and that it may be required from an early age. The mode of this contribution is unclear, but abnormal renal responses have been identified.
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PMID:Blood pressure and renal function in a novel vasopressin-deficient, genetically hypertensive rat strain. 279 78

The serum vasopressin (S-AVP) concentration, serum sodium concentration and osmolality, central venous pressure and fluid balance were measured during 10-min periods in 32 patients undergoing transurethral resection of the prostate. Concentration of S-AVP was unaffected by uncomplicated resection; irrigant absorption resulted in immediate increase in S-AVP concentration, but this increase could not explain the hypertension that occurred in some patients with absorption; a sudden decrease in the systolic arterial pressure was followed by a marked increase in S-AVP concentration; and extensive blood loss did not stimulate release of AVP, provided there was no associated arterial hypotension.
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PMID:Vasopressin responses during transurethral resection of the prostate. 280 90

The sequence of atrial natriuretic factor (ANF) has been determined, as well as the complete structure of the rat and human complementary DNA and gene. ANF and ANF messenger RNA are present not only in atria but also in ventricles. The circulating form of ANF has been identified as the C-terminal of the molecule, ANF (Ser 99-Tyr 126). The isolated secretory granules of rat atrial cardiocytes contain only pro-ANF (Asn 1-Tyr 126). An enzyme (IRCM-SP1) has been isolated from heart atria and ventricles. This enzyme is highly specific in cleaving ANF (Asn 1-Tyr 126), to yield ANF (103-126), (102-126), and (99-126). In target cells, ANF produces a rise in cyclic guanosine 3',5'-monophosphate (cGMP) due to activation of particulate guanylate cyclase, and inhibition of adenylate cyclase leading in some cases to a decrease in cyclic adenosine 3',5'-monophosphate (cAMP). ANF produces relaxation of rabbit and rat aortic strips, inhibits steroidogenesis in both zona glomerulosa and zona fasciculata cells, and inhibits the release of arginine vasopressin from the isolated rat hypothalamohypophysial preparation in vitro but decreases AVP release in vivo only at pharmacological doses. In all forms of experimental hypertension, plasma levels of ANF are increased and, at some time periods, atrial levels are also decreased. The ventricular levels of immunoreactive ANF are also increased in renal hypertension. Infusion of ANF by minipumps decreases the blood pressure near control levels in several models of experimental hypertension. In cardiomyopathic hamsters with heart failure, the atrial levels of immunoreactive ANF are decreased while the plasma and ventricular levels are increased.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Nov
PMID:The heart as an endocrine gland. 282 60

A syndrome of periodic catecholamine and prostaglandin E2 discharge is described in 2 patients aged 17 and 3 years. They had recurrent attacks of vomiting, hypertension and psychotic depression for several years with a fixed periodicity. At initiation of the attack, plasma ACTH, AVP, norepinephrine and prostaglandin E2 were markedly elevated, whereas dopamine was undetectable. This resulted in hypercortisolemia, hyponatremia and oliguria, which were completely normalized when the attack subsided. Dopaminergic inhibition by metoclopramide injection induced a sustained rise in plasma bicyclo-prostaglandin E2 in the patients, a transient rise in 4 controls, and no response in 8 control children. The 4 control responders had significantly higher plasma norepinephrine levels and aldosterone responses than the non-responders (P less than 0.001). There was a linear correlation between peak values of bicyclo-prostaglandin E2 and basal norepinephrine levels (r = 0.990, P less than 0.001). The patients released bicyclo-prostaglandin E2 and aldosterone more easily than the control responders in terms of plasma norepinephrine and dopamine levels. Treatment of the patient with clonidine was partially effective, whereas administration of indomethacin completely suppressed recurrence of the attacks for 1 year. These results suggest the etiologic possibility that the patients have a decreased dopaminergic inhibition of prostaglandin E2-mediated norepinephrine secretion, which causes periodic discharge of norepinephrine and concomitant release of ACTH and AVP.
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PMID:Recurrent attacks of vomiting, hypertension and psychotic depression: a syndrome of periodic catecholamine and prostaglandin discharge. 283 85

Pressor responses to vasopressin were determined in pigs and sheep during three experimental periods: 1) before deoxycorticosterone acetate (DOCA) treatment, 2) 21 days after DOCA implantation (100 mg/kg) when a stable hypertension had developed, and 3) after reversal of the hypertension by removing the implant in the sheep or by decreasing the dietary sodium intake in the pigs. The infusion of lysine (LVP) or arginine (AVP) vasopressin into pigs and sheep, respectively, resulted in dose-dependent increases in plasma vasopressin concentration. The levels of plasma LVP or AVP achieved by these infusions were not altered in any of the experimental periods. The administration of vasopressin resulted in dose-dependent increases in mean arterial blood pressure. However, pigs required five times more LVP than sheep required AVP to achieve similar pressor responses. The pressor responsiveness to vasopressin was attenuated when either species was made hypertensive. This effect was reversed when normal blood pressure was restored by reducing sodium intake in the pigs or by removing the DOCA implant from the sheep. These data establish that an increased pressor response to vasopressin does not contribute to DOCA hypertension in pigs or sheep.
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PMID:Pressor responses to vasopressin in pigs and sheep with DOCA hypertension. 291 71

This study compared the haemodynamic and arginine vasopressin responses of patients to fentanyl or sufentanil anaesthesia for coronary artery bypass surgery. Fourteen normotensive patients with normal left ventricular function were studied. Patients were induced with fentanyl (N = 7) 37.5 micrograms X kg-1 or sufentanil (N = 7) 7.5 micrograms X kg-1 by intravenous infusion over three minutes. Clinically important chest wall rigidity, bradycardia and recall of intraoperative events did not occur. All of the fentanyl patients became hypertensive after induction and five required vasodilator therapy since they did not respond to boluses of fentanyl (12.5 micrograms X kg-1). Two of these five patients had S-T depression greater than 1 mm. Five patients in the sufentanil group became hypertensive after induction. Four of these patients responded to additional sufentanil (3.75 micrograms X kg-1) while one required vasodilator therapy for concomitant S-T depression. Sufentanil attenuated the increase of arginine vasopressin during cardiopulmonary bypass. Levels of arginine vasopressin in the fentanyl group were significantly higher than those of the sufentanil group during bypass. Levels of AVP after bypass were higher in the sufentanil group. The incidence of hypertension was similar in both groups. The hypertension was more easily treated with sufentanil but concomitant vasodilators (nitroglycerine) were required in both patient groups. Neither fentanyl in doses up to 128 +/- 8.7 micrograms X kg-1 nor sufentanil in doses up to 23 +/- 1.4 micrograms X kg-1 can be used as sole agents for anaesthesia in adult coronary artery bypass patients with good ventricular function when induction times are three minutes and bolus top-up doses are used.
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PMID:Haemodynamic and plasma vasopressin responses during high-dose fentanyl or sufentanil anaesthesia. 294 80


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