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

In the present study, 52 patients with cirrhosis, portal hypertension, and variceal hemorrhage underwent either an elective or an emergency side-to-side portacaval shunt operation. Vasopressin was infused intravenously at 60 units/hour from just prior to abdominal incision until completion of the anastomosis. Eight of 35 patients who received vasopressin alone (23 percent) tolerated increased doses of 75 to 90 units/hour to obtain hemostasis. Four of 52 patients required simultaneous infusion of sodium nitroprusside to correct systemic hypertension. An additional 15 percent reduction in portal venous pressure occurred in these patients. Eleven of 13 patients with vasopressin-induced myocardial ischemia responded to simultaneous infusion of nitroglycerin. Further prospective studies are indicated to adequately delineate the dose and duration of therapy with either nitroprusside or nitroglycerin for simultaneous administration with intravenous vasopressin.
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PMID:Simultaneous infusion of nitroglycerin and nitroprusside to offset adverse effects of vasopressin during portosystemic shunting. 249 34

The aim of this study was to assess the hormonal alterations that may mediate the systemic hypertension that develops in patients during the perioperative period of orthotopic liver transplantation. We studied nine pediatric patients without previous hypertension or renal disease during six time points, starting before transplantation and ending at 48 hours after surgery. Hypertension developed in all patients in association with central venous pressures less than 10 mm Hg. Free water clearance was negative in all nine patients. Vasopressin levels increased intraoperatively but fell as hypertension developed. Atrial natriuretic factor levels increased as systemic blood pressure rose. A high level of plasma renin activity was observed in four patients with renal insufficiency. In six patients, postoperative 24-hour urinary norepinephrine excretion was within the normal age-adjusted range. These findings suggest that the combination of cyclosporine, corticosteroids, and, in some patients, an elevated plasma renin activity prevents the kidney from responding to the acute volume and salt overload with an appropriate diuresis and natriuresis, thus leading to systemic hypertension. The treatment of hypertension after liver transplantation may include salt restriction, diuretics, and, in those patients with a low creatinine excretion index, angiotensin coverting enzyme inhibitors.
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PMID:Mechanisms of hypertension during and after orthotopic liver transplantation in children. 252 74

To determine whether paraventricular nucleus (PVN) can play a role in the hypertension in DOCA/salt-treated rats, DOCA/salt hypertension was produced in PVN lesions and sham-operated rats. In lesioned rats, the development of hypertension was significantly attenuated (day 7: 132 +/- 3 v 157 +/- 5 mm Hg, P less than 0.01; day 14: 132 +/- 3 v 157 +/- 5 mm Hg, P less than 0.01; day 21: 189 +/- 2 v 224 +2- 6 mm Hg, P less than 0.01). Lesions lowered systolic blood pressure in even control rats. Mean blood pressure (mBP) from awake free moving rats was also significantly lower in lesioned DOCA/salt-treated rats than those of sham-operated DOCA/salt-treated rats (155 +/- 14 mm Hg v 193 +/- 13, P less than 0.01), while mBP was not different between lesioned and sham-operated control rats. The reduction of mBP by hexamethonium injections was significantly larger in sham-operated DOCA/salt-treated rats than those of lesioned DOCA/salt rats. (-53 +/- 3% v -45 +/- 2, P less than 0.05). Plasma norepinephrine and epinephrine were significantly elevated in DOCA/salt-treated rats, however, PVN lesions inhibited significantly those elevations. 1-Deaminopenicillamine, 4-valine, 8-D-arginine Vasopressin (dPVDAVP) injections did not affect BP and heart rate in all rats. Body weight, water intake, urine volume, urine Na, K, and vasopressin excretion, and urine osmorality were not altered by lesions. These findings suggest that PVN contributes to development of hypertension in DOCA/salt-treated rats with sympathetic nervous activations.
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PMID:Paraventricular nucleus lesions attenuate the development of hypertension in DOCA/salt-treated rats. 257 May 97

The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. Vasopressin-deficient, vasopressin-synthesizing and vasopressin-deficient rats chronically supplemented with deamino-8-D-arginine vasopressin (dDAVP) were compared with water-drinking controls. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. The development of DOCA-salt hypertension was attenuated in the vasopressin-deficient rats, which had a similar level of total body water, slightly increased intracellular water and significantly decreased extracellular fluid volume compared with the hypertensive vasopressin-synthesizing rats. Consequently, in the vasopressin-deficient rats, the ratio of extracellular fluid volume to intracellular water did not differ from that of controls. A vasopressin deficiency was associated with a failure to expand the interstitial fluid volume although plasma volume was increased. Unaltered total body water together with elevated plasma osmolality indicated an extracellular water deficiency in DOCA-salt-treated vasopressin-deficient rats. Chronic dDAVP supplementation restored the body fluid pattern and the hypertensive response of the DOCA-salt-treated vasopressin-deficient rats. In conclusion, the antidiuretic effects of vasopressin are necessary for the interstitial fluid volume expansion that is essential for a full development of DOCA-salt hypertension.
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PMID:Vasopressin and water distribution in rats with DOCA-salt hypertension. 263 18

1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium. 2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist. 3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished. 4. Adrenaline infused intravenously to mimic the levels that occurred after morphine caused a similar degree of hyperglycaemia but only a small increase in blood pressure. 5. Pretreatment with intracerebroventricular naloxone prevented the morphine-induced hypertension, hyperglycaemia, increase in plasma catecholamines, respiratory depression and sedation. 6. These results demonstrate that, in conscious rabbits, intravenous morphine causes hypertension by increasing sympathetic vasoconstrictor nerve activity and elevating plasma adrenaline levels; the latter alone produces the hyperglycaemia. Vasopressin release is not involved in the hypertensive response to morphine. The effects of morphine appear to result from stimulation of central opiate receptors leading to enhanced sympathoadrenal outflow.
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PMID:Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits. 271 53

This study was performed to characterize and quantify vasopressin in neuron-enriched primary cultures of whole brains from 1-day-old rats and to compare such cultures between spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Vasopressin was extracted from cells and evaluated by radioimmunoassay and high-pressure liquid chromatography. Radioimmunoassay of high-pressure liquid chromatography fractions from cell extracts showed that the major peak of immunoreactivity comigrated with synthetic vasopressin. Cell vasopressin content increased in a graded manner when one to six dishes (plated 8 x 10(6) cells/dish) were pooled (8.7 +/- 0.5 to 67.7 +/- 8.2 pg/dish). When the number of plated cells per dish was increased (2 to 16 x 10(6) cells), there was also a graded rise in dish vasopressin content (3.4 +/- 0.4 to 15.3 +/- 3.9 pg). Treatment of cultures with 100 aM to 1 nM of angiotensin II for 5 minutes caused a dose-dependent decrease in cell vasopressin content. Furthermore, the decrease in cell vasopressin content of cultures treated with 1 nM angiotensin II (12.6 +/- 0.8 to 7.0 +/- 1.0 pg/10(6) cells, p less than 0.05) corresponded with the increase in medium vasopressin concentration (3.8 +/- 0.5 to 7.5 +/- 2.3 pg/ml) and this vasopressin-releasing effect of angiotensin II was blocked by [Sar1, Thr8]angiotensin II. Treatment of cultures with potassium chloride (56 mM) and acetylcholine chloride (5.5 microM) also resulted in significant decreases in cell vasopressin content.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Jun
PMID:Vasopressin in neuronal cultures from neonatal rat brain. 273 28

Antidiuretic hormone is known to stimulate the renal synthesis of prostaglandins. These autacoids, in turn, modulate the pressure natriuresis phenomenon. Accordingly, the present study was done to test the hypothesis that, in the absence of antidiuretic hormone and antidiuretic hormone-dependent prostaglandin synthesis, the pressure natriuresis response is blunted. Experiments were performed on Brattleboro diabetes insipidus rats (n = 7) and Long Evans control rats (n = 14). A change in perfusion pressure in the Long Evans rats from 89.3 +/- 1.0 to 108.7 +/- 1.1 mm Hg (p less than 0.05) was associated with significant increases in the fractional excretion of sodium (1.1 +/- 0.2 to 2.3 +/- 0.3%) and the urinary prostaglandin excretion (32.6 +/- 6.8 to 56.6 +/- 10.0 pg/min). In contrast, a similar change in perfusion pressure in the diabetes insipidus rat from 88.6 +/- 1.4 to 106.2 +/- 1.5 mm Hg (p less than 0.05) resulted in no significant increases in either sodium or prostaglandin excretions. Treatment of a third group of diabetes insipidus rats (n = 9) with 1-desamino-8-D-arginine vasopressin (1 microgram/day) restored the natriuretic response to increases in renal perfusion pressure. Treated diabetes insipidus and Long Evans control rats had comparable natriuretic responses to increases in renal perfusion pressure. Untreated diabetes insipidus rats, on the other hand, had blunted responses. In summary, the pressure natriuresis response in diabetes insipidus rats is blunted compared with Long Evans control rats. We conclude that antidiuretic hormone is necessary for the complete expression of the pressure natriuresis response.
Hypertension 1989 Apr
PMID:Blunted pressure natriuresis in the Brattleboro diabetes insipidus rat. 292 34

Recently, there has been an explosion of knowledge on vasopressin, including its neuro-anatomy, biochemistry and physiology. Recent work demonstrates extensive extra-hypothalamic vasopressinergic projections from the SON and PVN. Of particular importance are projections to the cardiovascular medullary centres. Conversely, the SON and PVN receive reciprocal catecholaminergic innervation from autonomic medullary centres. Vasopressin should now be regarded as a peptide hormone with important peripheral effects, as well as a neuropeptide acting as a neurotransmitter or neuromodulator with important CNS actions. The central and peripheral vasopressin systems are not only anatomically differentiated, but, although integrated, may also function independently. There is an important interaction between the central vasopressin system and the autonomic nervous system. Vasopressin has multiple and diverse actions on the cardiovascular system, including direct vasoconstriction, antidiuresis and hence volume control, central actions on cardiovascular neural centres, modulation of the baroreflex and direct cardiac effects. It also acts in concert with the sympathetic nervous system and the renin-angiotensin system as an integrated neurohormonal system in the control of blood pressure. Vasopressin appears to have an important role as a vasoconstrictor agent whenever volume is threatened, such as in dehydration, haemorrhage, adrenal insufficiency and orthostasis. It seems unlikely that vasopressin acts as a direct vasoconstrictor agent in the pathogenesis of any form of experimental or human hypertension. Although plasma vasopressin levels have been reported to be elevated in most forms of hypertension, this correlates best with the severity of hypertension. Furthermore, the levels are not elevated to the pressor range, so that increased vascular reactivity and sensitivity has to invoked. This does not appear to be specific for vasopressin. However, vasopressin may be indirectly involved through volume maintenance or interactions within the CNS. Indeed, its volume retaining properties have probably been underestimated. Whereas in acute situations the vasoconstrictor properties may be of some importance, it is difficult to sustain long-term hypertension without maintenance of an adequate plasma volume. Vasopressin's central actions on the cardiovascular medullary centres, the baroreflex, the autonomic nervous system and catecholamine metabolism may also be involved in some hypertensive processes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vasopressin in circulatory control and hypertension. 293 70

Manipulations of salt and water intake influenced the atriopeptin content in the atria and plasma of rats. Plasma levels of atriopeptin varied in proportion with dietary salt intake. In contrast, cardiac levels of atriopeptin varied inversely with the amount of salt in the diet. Acute stimulation of atriopeptin release can be produced by treatments which elevate atrial pressure, including atrial stretch, volume overloading, water immersion, and vasoconstrictor agents. Vasopressin-stimulated atriopeptin release preferentially depleted right atrial stores. In spite of the initial differences in cardiac stores of atriopeptin in the rats on different diets, there were no major differences in the amount of atriopeptin released in response to vasopressin stimulation. These data suggest that there is a functional excess of cardiac atriopeptin stores. We also examined the atrial and plasma atriopeptin content in the Dahl salt-sensitive and resistant rats to determine whether the development of hypertension in the Dahl sensitive rats is associated with abnormalities in basal or stimulated levels of atriopeptin. The effects of dietary salt intake on basal and stimulated atriopeptin levels in both the Dahl sensitive and resistant rats were similar to those observed in normal rats, suggesting that abnormalities in atriopeptin content do not contribute to the etiology of hypertension in the Dahl salt-sensitive rat.
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PMID:Atriopeptin release in conditions of altered salt and water balance in the rat. 294 44

Cells were isolated from the outer medulla of the rabbit kidney, primarily from the thick ascending limb of Henle's loop (mTALH). These mTALH cells are heavily invested with a cytochrome P450-linked monooxygenase that represents the third pathway by which arachidonic acid is metabolized. After cell separation, approximately 80% of the cells proved to be mTALH in origin, based on electron microscopic criteria and immunofluorescent localization of Tamm-Horsfall protein, a specific marker for mTALH cells. The specific activity of alkaline phosphatase, a marker for proximal tubular cells, decreased threefold after separation of mTALH cells from outer medullary cells, associated with a fourfold increase in the capacity of the separated mTALH cells to metabolize arachidonic acid. Incubation of mTALH cells with 14C-arachidonic acid resulted in formation of oxygenated metabolites, identified as two peaks (P1 and P2), which accounted for 30 to 40% of the recovered radioactivity. Formation of prostaglandin E2 and F2 alpha accounted for only 3 to 5%. The chromatographic retention times of P1 and P2 were different from products of lipoxygenases. An inhibitor of cytochrome P450-dependent enzymes, SKF-525A (50 microM), reduced product formation by mTALH cells by more than 70%, while induction of cytochrome P450 increased product formation. Formation of P1 and P2 by cell-free homogenates of mTALH was totally dependent on the presence of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH), which suggests a NADPH-dependent cytochrome P450-linked monooxygenase pathway. Vasopressin and calcitonin (10(-10) M to 10(-7) M) stimulated release of arachidonic acid metabolites from mTALH cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Renal arachidonic acid metabolism. The third pathway. 298 23


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