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

To assess the mechanism responsible for maintaining the elevated arterial pressure in 2-kidney DOCA treated Yucatan miniature swine, cardiovascular parameters and the responses to hexamethonium bromide (HMB) were evaluated in normal and DOCA treated animals. Using chronically instrumented conscious animals, measurements of mean arterial pressure (MAP), cardiac output (CO), and calculated total peripheral resistance (TPR) revealed that with DOCA hypertension MAP was increased 50-60 mmHg above controls. This increased pressure was due to an increase in TPR with CO remaining normal. HMB normalized the MAP of the DOCA animals via a selective lowering of TPR to a value similar to that of the controls. In DOCA hypertensive animals these functional changes, due to increased peripheral sympathetic nerve activity, were reflected by significantly elevated plasma norepinephrine. In this animal DOCA administration produces a neurogenic form of hypertension which appears to be analogous to essential hypertension in man.
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PMID:The role of the sympathetic nervous system in 2-kidney DOCA-hypertensive Yucatan miniature swine. 287 9

We tested the hypothesis that the antihypertensive effects of dietary taurine supplementation in deoxycorticosterone acetate (DOCA)-salt rats may be attributed to the suppression of sympathetic nervous system activity. In uninephrectomized rats treated with DOCA while receiving 1% NaCl solution for 2 weeks, systolic blood pressure was significantly increased as compared with that in control rats treated with vehicle suspension and tap water. Sympathetic nervous system activity was assessed by tissue norepinephrine turnover, which was determined from the rate of decline of tissue norepinephrine concentration after the administration of alpha-methyl-p-tyrosine, a potent inhibitor of the rate-limiting step of catecholamine synthesis. Cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure (4 degrees C, 8 hours) were markedly increased in DOCA-salt rats as compared with control rats. Also, DOCA-salt rats had increased depressor response to hexamethonium bromide, a ganglion blocker. In contrast, supplementation of 1% taurine in DOCA-salt rats attenuated the development of the hypertension associated with the normalization of both the increased depressor response to ganglionic blockade and the accelerated cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure. Taurine supplementation in control rats, however, had no effect on blood pressure or norepinephrine turnover during cold exposure. These results suggest that taurine supplementation suppresses sympathetic overactivity in DOCA-salt rats, thus leading to inhibition of the development of hypertension.
Hypertension 1987 Jan
PMID:Role of sympathetic nervous system in hypotensive action of taurine in DOCA-salt rats. 287 80

This study was carried out on 12 patients (mean age 61) in order to assess the oxygen consumption (VO2) in the post-operative stage of an elective surgical procedure (replacement of the abdominal aorta). Anesthesia was a combination of thiopentone, pancuronium bromide and high doses of droperidol and fentanyl. Patients were kept intubated and ventilated in the post-operative period. VO2 and other related metabolic parameters as well as hemodynamic parameters were measured every 45 minutes over a period of 5 hours. A VO2 increase (127%) related to the increase in body temperature was noted. Mean VO2 for all patients during the whole period was 170 +/- 13 ml.min-1.m-2 (range: 51-411 ml.min-1.m-2). Mean value of maximal VO2 was 240 +/- 21 ml.min-1.m-2 (range: 1471-411 ml.min-1.m-2). Large dose of droperidol are shown to limit VO2 increase. In patients with shivering, the maximal value of VO2 was found during shivering. The amount of droperidol administered during anesthesia was greater in patients without shivering. VO2 increase was due to a rise in tissular O2 extraction. Cardiac index was insufficiently increased (+ 9.4%) and a certain extent of myocardial inadaptability was suspected in relation with: high blood pressure, hypovolaemia and/or myocardial effect of anesthesia agents.
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PMID:[Hemodynamic and gasometric modifications during the anesthesia recovery period in patients undergoing ventilation after surgery of the abdominal aorta]. 292 87

Inhibition of cardiovascular Na,K-pump activity has been shown to promote an increase in the contractile activity of myocardial and vascular smooth muscle and a consequent rise in blood pressure (BP). It has also been shown that vascular Na,K-pump activity and myocardial Na+K+ATPase activity [the energy source for active sodium (Na) and potassium (K) transport] are decreased in rats with various forms of low renin hypertension including rats with reduced renal mass-saline (RRM-saline) hypertension. In the present study, left ventricular Na+K+ATPase activity from rats with RRM-saline hypertension was found to be decreased in membranes prepared by two independent methods: deoxycholate, sodium iodide (Nal)-treated microsomal fractions (method 1) and membranes prepared by the hypotonic, lithium bromide (LiBr) method (method 2). Relative to RRM normotensive control rats which drank distilled water, myocardial Na+K+ATPase activity from RRM-saline drinking rats was decreased by 18.2% in membranes prepared by method 1 and 33.6% in membranes prepared by method 2. The apparent affinities of Na+K+ATPase for K and for ouabain were unaltered relative to controls in membranes prepared from these hypertensive rats by method 1, and the sialic acid content and 5'-nucleotidase activity (two putative sarcolemmal markers) were unaltered in membranes from the hypertensive rats, prepared by methods 1 and 2 respectively. The Mg2+ATPase activity of membranes prepared by method 1 was increased in the RRM-saline hypertensive rats but because it was not increased in membranes prepared by method 2 the former observation does not appear to be of any pathophysiological importance. In other experiments, hypertension was reversed in RRM-saline hypertensive rats by restricting their salt intake (substitution of distilled water for drinking).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased myocardial Na+K+ATPase activity in rats with reduced renal mass-saline hypertension. 300 89

3-Mercaptopropionic acid (3-MP), an inhibitor of the synthesis of GABA, acts in the central nervous system to increase arterial pressure (+50-60 mmHg) in anesthetized guinea pigs, apparently by sympathoadrenal activation. However, blockade of nicotinic receptors in autonomic ganglia with hexamethonium (10 or 20 mg/kg, i.v.) failed to effect any degree of sustained reversal of increases in blood pressure. Infusion of atropine methyl bromide (1 mg/kg, i.v.) likewise was without effect when administered alone, but completely reversed the hypertension induced by 3-MP when given after treatment with hexamethonium. These findings suggest that ganglionic transmission through either the "classical" nicotinic pathway or a muscarinic pathway is sufficient to sustain the sympathetically-mediated pressor response elicited by 3-MP.
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PMID:Evidence for transmission through sympathetic ganglia mediated by muscarinic receptors in anesthetized guinea pigs. 301 88

Prostaglandin I2 (PGI2) is known to stimulate ventricular C fiber receptors resulting in a Bezold-Jarisch-like reflex. Also, cardiac receptor stimulation is known to interact with the expression of arterial baroreflexes. Therefore, experiments were performed to determine the effects of left circumflex coronary artery infusion of PGI2 on the baroreflex control of heart rate in conscious instrumented dogs. Dogs were instrumented chronically with an aortic catheter for the measurement of mean aortic pressure, hydraulic occluder cuffs on the descending aorta and inferior vena cava, a left ventricular catheter for the measurement of left ventricular pressure and heart rate, and a nonocclusive catheter in the left circumflex coronary artery. At the time of experimentation, arterial pressure was altered randomly in steps by partially inflating the occluders. Mean arterial pressure-heart curves (baroreflex curves) were constructed by fitting the data to a logistic curve by nonlinear regression. PGI2 infused into the left circumflex coronary artery at doses of 10, 20, and 50 ng/kg/min caused significant (p less than 0.05) inhibition of the maximum heart rate, heart rate range, and maximum slope of the curve compared to the control baroreflex curve obtained during intracoronary infusion of PGI2 vehicle. PGI2 had no significant effect on the minimum heart rate during hypertension. Since PGI2 is known to stimulate left ventricular receptors, these effects were most likely produced via stimulation of cardiac receptors. In additional experiments using beta 1-blockade with metoprolol or cholinergic blockade with atropine methyl bromide, it was shown that PGI2 attenuates baroreflex-mediated tachycardia by preventing parasympathetic withdrawal completely and by attenuating sympathetic stimulation by approximately 50%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracoronary infusion of prostaglandin I2 attenuates arterial baroreflex control of heart rate in conscious dogs. 305 4

It is evident that hypertension is associated with elevated endogenous opiates. This study was designed to examine the role of endogenous opiates in the development and/or maintenance of two-kidney renovascular hypertension and in baroreceptor reflex function in conscious hypertensive rats. Naloxone administration during the onset of hypertension significantly attenuated the rise in blood pressure. After one week, systolic blood pressure in naloxone-treated rats was 27 mmHg lower than in 0.9% NaCl-treated hypertensive rats. Acute naloxone infusions in chronic hypertensive animals also significantly lowered blood pressure (-10%) and heart rate (-26%). Baroreceptor function was significantly enhanced in both normotensive (+135%) and hypertensive (+207%) rats after administration of naloxone. Furthermore, naloxone treatment also caused the baroreflex response to shift from the higher reset state toward that seen in normotensive counterparts. The inability of naloxone methyl bromide to alter baroreflex sensitivity indicates that the site(s) of action of opiates resides in the brain. These data support a role for opiates in the development and/or maintenance of renovascular hypertension, which may be related to alterations in baroreceptor reflex function.
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PMID:Endogenous opiate modulation of baroreflexes in normotensive and hypertensive rats. 318 85

The intracranial pressure (ICP) irregularities, i.e., pressure waves, were studied in dogs with experimental subarachnoid hemorrhage. Animals were lightly anesthetised, immobilised with panchronium bromide and respirated artificially. Subarachnoid infusion of hemolysed red blood cells was used to induce intracranial hypertension. Recordings of both systemic blood pressure (SBP) and ICP were undertaken continuously. After the infusion of hemolysed blood the ICP increased gradually and reached to 50 mmHg or more at the terminal stage. The pressure waves were classified into two types, i.e., the fast waves and the slow waves. The fast waves had a duration of 10-30 seconds, being accompanied by a marked increase of the SBP. The slow waves gradually increased their frequency and the duration, when the ICP increased more than 20 mmHg or more resembling plateau-like waves. Postmorten examination showed hemogenic meningitis at the base of the brain, especially the medulla oblongata. The results suggest that studies of the slow waves is of value for analyzing plateau waves.
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PMID:[Intracranial pressure irregularities in experimental subarachnoid hemorrhage]. 395 62

Recent studies have demonstrated a hypoalgesia in hypertensive subjects. This study reports and evaluates factors responsible for the expression of the hypoalgesic behavior demonstrated by genetically hypertensive rats of the Okamoto-Aoki strain (SHR) as compared to normotensive age-matched Wistar-Kyoto rats (WKY). Analgesiometric assays were conducted by the hot plate method. SHR's hypoalgesic behavior was reversed by subcutaneously administered naloxone. The intravenous administration of naloxone did not alter arterial pressure or heart rate in either SHR or WKY. Subcutaneous administration of the peripherally acting ganglionic blocker hexamethonium bromide at a dose which lowered mean arterial blood pressure and thus decreased tonic baroreceptor stimulation, concomitantly reversed the SHR hypoalgesic behavior and induced a hyperalgesia in WKY. Denervation of the sino-aortic baroreceptors failed to alter the hypoalgesic behavior demonstrated by SHR. Denervation of the right vagal nerve trunk with associated cardiopulmonary baroreceptor afferents resulted in a reduction of the SHR hypoalgesic behavior and produced a hyperalgesic behavior in WKY as compared to age-matched sham operated controls over a 4 week period. These data suggest a possible physiological role for vagal afferent systems in the concomitant regulation of resting arterial blood pressure and responsiveness to aversive environmental stimuli. A discussion of the interaction between blood pressure and pain regulatory systems as potential substrates associated with the onset and maintenance of hypertension is provided.
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PMID:Factors influencing the altered pain perception in the spontaneously hypertensive rat. 612 88

Increased sympathetic nervous system activity has been demonstrated in established one-kidney one-clip hypertension in the rat. We have found that renal denervation in this model results in an attenuation of hypertension, unassociated with alterations in sodium or water balance or renin activity. To determine whether the depressor effect of renal denervation is associated with changes in peripheral sympathetic nervous system activity, sham operation (n = 12), renal denervation (n = 13), or unclipping (n = 13) was carried out 2 wk after the onset of one-kidney one-clip hypertension. Normotensive unine-phrectomized age- and sex-matched rats were used as controls (n = 14). Renal denervation resulted in a significant decrease in systolic blood pressure (201+/-7 to 151+/-6 mm Hg), while unclipping lowered systolic blood pressure to normotensive levels (130+/-6 mm Hg). 8 d after operation plasma norepinephrine and mean arterial pressure before and after ganglionic blockade with 30 mg/kg hexamethonium bromide were measured in conscious, unrestrained, resting animals, as indices of peripheral sympathetic nervous system activity. Plasma norepinephrine was significantly higher in hypertensive sham-operated rats (422+/-42 pg/ml) compared with normotensive controls (282+/-25 pg/ml) (P < 0.01). Both renal denervation and unclipping restored plasma norepinephrine to normal levels (273+/-22 and 294+/-24 pg/ml, respectively). Ganglionic blockade in hypertensive sham-operated animals resulted in a significantly greater decrease in mean arterial pressure than occurred in renal denervated, unclipped, or control rats. The data suggest that the depressor effect of renal denervation or unclipping in the one-kidney one-clip hypertensive rat is associated with a decrease in peripheral sympathetic nervous system activity.
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PMID:Decrease in peripheral sympathetic nervous system activity following renal denervation or unclipping in the one-kidney one-clip Goldblatt hypertensive rat. 617 49


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