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

In acute gastrointestinal bleeding visceral angiography has been showing its importance for years. It contributes to diagnosis especially in cases with persistent acute hemorrhage. In chronic gastrointestinal bleeding conventional radiographic procedures such as upper gastrointestinal series and barium enema will be preferred to angiography. The function of the radiologist goes beyond mere diagnosis of gastrointestinal bleeding. Treatment with vasopressin via the angiographic catheter has proven its clinical value. This method will be indicated especially in cases with high risk anesthesia and surgery. It will help to postpone necessary surgery to a more favorable moment following hemostasis. Side effects such as hypertension and antidiuresis are relatively rare and easy to manage. Numerous substances are used for embolization showing that ideal material has not been found yet and further development seems necessary. In contrast to vasopressin treatment, vascular occlusion is often irreversible, complications (unwanted reflux of embolization material, necrosis and plugging of the catheter) are more difficult to manage. Superselective visualization of a bleeding artery is always needed. Embolization is justified in cases when a possibility for anesthesia and surgery cannot be foreseen. The electrical vascular occlusion using direct current is still in the phase of animal experiments; its clinical value has not sufficiently been assessed as yet.
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PMID:[Angiographic diagnosis and therapy of acute and chronic gastrointestinal hemorrhages]. 30 84

Clinical states with portal venous hypertension are frequently associated with impairment in renal hemodynamics and water excretion, as well as increased renin secretion. In the present investigation, portal venous pressure (PVP) was increased in anesthetized dogs undergoing a water diuresis. Renal arterial pressure was maintained constant in all studies. As PVP was increased from 6 to 20 mm Hg, decreases in cardiac output (2.5-2.0 liter/min, P less than 0.05) and mean arterial pressure (140-131 mm Hg, P less than 0.05) were observed. Increases in PVP were also associated with decreases in glomerular filtration rate (GFR, 40-31 ml/min, P less than 0.001), renal blood flow (RBF, 276-193 ml/min, P less than 0.001), and increases in renin secretion (232-939 U/min, P less than 0.025) in innervated kidneys. No significant change in either GFR or RBF and a decrease in renin secretion occurred with increases in PVP in denervated kidneys. To dissociate the changes in cardiac output and mean arterial pressure induced by increase PVP from the observed decreases in GFR and RBF, studies were performed on animals undergoing constriction of the thoracic inferior vena cava. In these studies, similar decreases in cardiac output and mean arterial pressure were not associated with significant changes in GFR or RBF. Increases in PVP also were associated with an antidiuresis as urine osmolality increased from 101 to 446 mosmol/kg H2O (P less than 0.001). This antidiuresis was significantly blunted but not abolished by acute hypophysectomy. In hypophysectomized animals, changes in free water clearance and urine flow were linearly correlated as PVP was increased. These studies indicate that increases in PVP result in decreases in GFR and RBF and increases in renin secretion mediated by increased renal adrenergic tone. Increased PVP is also associated with antidiuresis; this antidiuresis is mediated both by vasopressin release and by diminished tubular fluid delivery to the distal nephron.
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PMID:Mechanisms of portal hypertension-induced alterations in renal hemodynamics, renal water excretion, and renin secretion. 96 99

Endothelium-derived relaxing factor (EDRF) activates soluble guanylate cyclase, resulting in an increase in vascular smooth muscle guanosine 3',5'-cyclic monophosphate (cGMP) levels, which correlates with its relaxing effect. Using a microdialysis technique, we investigated changes in right and left renal interstitial fluid cGMP levels in response to right intrarenal administration of an EDRF inhibitor, NG-monomethyl-L-arginine (L-NMMA). Studies were conducted in anesthetized dogs (n = 5) in metabolic balance at a sodium intake of 40 meq/day. Urine was collected directly from the right and left ureters individually. Changes in the right and left urinary cGMP excretion and renal function in response to cumulative doses of L-NMMA were studied. In the right kidney, 20-100 micrograms/kg/min L-NMMA caused 1) a dose-dependent decrease in renal interstitial fluid and urinary cGMP levels (p less than 0.0001 and p less than 0.001, respectively), 2) antinatriuresis (p less than 0.01), 3) antidiuresis (p less than 0.01), 4) a decrease in renal blood flow (p less than 0.01) and glomerular filtration rate (p less than 0.01), and 5) a decrease in fractional sodium excretion (p less than 0.01). No changes in left renal interstitial fluid and urinary cGMP levels or excretory and hemodynamic function were observed during right intrarenal administration of L-NMMA at 20 and 60 micrograms/kg/min.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Nitric oxide alters renal function and guanosine 3',5'-cyclic monophosphate. 131 56

A 63-year-old white female who was being treated for hypertension with lisinopril presented with seizures, altered mental status, and a serum sodium of 101 mEq/L. Serum sodium prior to initiation of lisinopril therapy was 137 mEq/L. The hyponatremia was corrected and did not recur after lisinopril was stopped. The hyponatremia may have been a result of polydipsia and inappropriate antidiuresis secondary to ACE-inhibitor therapy.
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PMID:Case report: severe symptomatic hyponatremia associated with lisinopril therapy. 131 75

Selective alpha-adrenoceptor and calcium antagonists have been used to determine both the alpha 1-adrenoceptor subtype and the extracellular calcium requirement for renal nerve-mediated antinatriuresis and antidiuresis in deoxycorticosterone acetate (DOCA)-salt and two-kidney, one clip (2K1C) Goldblatt hypertensive rats. Stimulation of the renal nerves at low frequencies reduced urine flow and absolute and fractional sodium excretions by 40-60% in pentobarbitone anaesthetized control, sham-operated, DOCA-salt and 2K1C Goldblatt hypertensive rats. Administration of prazosin, but not idazoxan, inhibited the renal nerve-induced excretory responses in both models of hypertension, a result compatible with the involvement of alpha 1-adrenoceptors. By contrast, the calcium antagonist inhibited the renal nerve-dependent antinatriuresis and antidiuresis in DOCA-salt but not 2K1C Goldblatt hypertensive rats. These results showed that the renal nerves mediated their action via alpha 1-adrenoceptors, but that the postreceptor responses were dependent on extracellular calcium in DOCA-salt but not 2K1C Goldblatt rats.
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PMID:The characteristics of alpha-adrenoceptors mediating the renal nerve induced antinatriuresis and antidiuresis in hypertensive rats. 164 65

The interaction between genetic and environmental factors is important in the pathophysiology of hypertension. By examining the effects of two environmental factors--acute psychoemotional stress and dietary sodium intake--in rats with genetic hypertension, an important influence on central neural mechanisms governing the renal sympathetic neural control of renal function has been demonstrated. Additional studies of the central opioid systems have demonstrated an important role of opioid peptides in modulating the renal functional responses to acute psychoemotional stress. The observed renal functional alterations--antidiuresis, antinatriuresis, and renal vasoconstriction--are known to be capable of contributing to the initiation, development, and maintenance of the hypertensive process.
Hypertension 1991 Apr
PMID:Stress and sodium intake in neural control of renal function in hypertension. 184 2

It has been hypothesized that moderately increased blood levels of arginine vasopressin (AVP) contribute to the development and/or maintenance of hypertension. In this study, male Sprague-Dawley rats on a fixed 1 meq daily sodium intake received 10-day intravenous infusions of 0.2 and 2.0 ng.kg-1.min-1 AVP. The higher infusion rate was above the acute vasoconstrictor threshold for AVP administration and also produced a maximal antidiuretic effect. During chronic AVP administration, however, daily mean arterial pressure, heart rate, and body fluid composition were not changed, despite a maintained antidiuresis. To test the hypothesis that circulating AVP failed to cause hypertension as a result of sensitization of the baroreflex or a direct sympathoinhibitory effect of the peptide, additional experiments were performed in rats subjected to sinoaortic denervation (SAD) or ablation of the area postrema (APX). Infusion of AVP for 10 days into SAD or APX rats caused a sustained antidiuresis but did not change arterial pressure, heart rate, or body fluid composition. In all groups of rats, the depressor response to ganglionic blockade (20 mg/kg hexamethonium) was used to estimate the autonomic component of resting arterial pressure; no change in autonomic cardiovascular control was found using this method in any of the groups during AVP infusion. Long-term elevation of plasma AVP in rats, therefore, does not cause hypertension or significantly affect autonomic regulation of arterial pressure.
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PMID:Effect of circulating vasopressin on arterial pressure regulation in rats. 256 56

To identify a physiological role for renal alpha 2 adrenergic receptors, renal vascular and tubular responses to administration of graded frequencies of renal nerve stimulation or graded doses of adrenergic agonists were determined in anesthetized spontaneously hypertensive, Wistar-Kyoto, and Sprague-Dawley rats. Renal vasoconstrictor responses to renal nerve stimulation and alpha 1-adrenergic receptor agonists (norepinephrine, phenylephrine) were inhibited by an alpha 1-adrenergic receptor antagonist (prazosin) but not by an alpha 2-adrenergic receptor antagonist (rauwolscine). A semilog plot of renal vasoconstrictor responses a fraction of control renal blood flow versus agonist dose (in nanograms) was linear with the slope, k, taken as the fractional decrease in renal blood flow per nanogram. The alpha 2-adrenergic receptor agonists (clonidine, guanabenz) produced minimal renal vasoconstrictor responses (fractional decrease in renal blood flow per nanogram: norepinephrine, 0.011; phenylephrine, 0.003; clonidine, 0.00087; guanabenz, 0.000037). The small renal vasoconstrictor responses to clonidine and guanabenz were more inhibited by rauwolscine than by prazosin. Low frequency renal nerve stimulation produced antidiuresis and antinatriuresis without decreasing glomerular filtration rate or renal blood flow. The antidiuretic and antinatriuretic responses were inhibited by prazosin but unaffected by rauwolscine. The magnitude of the renal vascular and tubular responses and their adrenergic receptor mediation were not different between spontaneously hypertensive, Wistar-Kyoto, and Sprague-Dawley rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Jan
PMID:Role of renal alpha 2-adrenergic receptors in spontaneously hypertensive rats. 287 79

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

1. An investigation was undertaken to examine the effect of calcium channel blockade, induced by amlodipine, on the ability of the renal sympathetic nerves to cause an antidiuresis and anti-natriuresis in normotensive Sprague Dawley and spontaneously hypertensive rats anaesthetized with pentobarbitone. 2. Low frequency renal nerve stimulation in normotensive rats, which did not change renal blood flow, caused a 15% reduction in glomerular filtration rate and was associated with falls in urine flow of 37%, absolute sodium excretion of 47%, and fractional sodium excretion of 38%. The magnitude of these renal excretory changes was unaffected by prior administration of amlodipine at either 200 micrograms kg-1 plus 50 micrograms kg-1 h-1 or 400 micrograms kg-1 plus 100 micrograms kg-1 h-1. Amlodipine given in the higher dose, decreased basal levels of blood pressure and increased basal urine flow and sodium excretion. 3. In spontaneously hypertensive rats, renal nerve stimulation minimally affected renal haemodynamics but decreased urine flow, absolute and fractional sodium excretion by 29%, 31% and 24%, respectively. 4. Similar renal nerve stimulation in spontaneously hypertensive rats given amlodipine at 200 micrograms kg-1 plus 50 micrograms kg-1 h-1 or 400 micrograms kg-1 plus 100 micrograms kg-1 h-1 caused minimal changes in renal haemodynamics and in the excretion of water and sodium. The higher dose of drug resulted in decreased blood pressure and increased basal rates of urine flow and sodium excretion. 5. These data show that in spontaneously hypertensive rats but not normotensive rats, calcium channel blockade inhibited the ability of the renal nerves to stimulate the reabsorptive processes for sodium at the renal tubule. This indicated that in spontaneous hypertension the post-receptor mechanisms had changed and become more dependent on the inward movement of calcium.
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PMID:A study of the action of amlodipine on adrenergically regulated sodium handling by the kidney in normotensive and hypertensive rats. 296 97


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