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

Baroreflex sensitivity (BRS) has not been assessed in coarctation, though it is diminished in renal and essential hypertension. Previous experimental studies of coarctation have dealt primarily with renal mechanisms of hypertension, and have relied on constricting the aorta in adult animals. We banded the thoracic aorta in newborn puppies, and performed studies 2 yr later. Blood pressure (BP) elevations, abundant chest wall collaterals, the absence of heart failure, and subsequent necropsy confirmed the full syndrome of natural coarctation in all dogs. Transient BP elevations were induced in conscious, unrestrained dogs with intravenous phenylephrine injections. Reflex bradycardia was quantitated by plotting each pulse interval in microseconds against BP of the preceding beat, and expressing BRS as the linear regression coefficient (slope) in ms/mmHg. Mean BRS in 10 dogs with coarctation did not differ significantly (P greater than 0.1) from 8 normal controls. Carotid sinus diameter (CSD) was also assessed. Carotid arteries were fixed in vivo by prolonged exposure to glutaraldehyde to prevent contraction, then were excised and measured in a calibrated microscope. Mean CSD in 10 dogs with coarctation was significantly greater (P less than 0.01) than in 10 control dogs. The unexpectedly normal BRS in experimental coarctation may be due to changes in CSD induced by hypertension; such changes may only develop in growing animals. Experimental studies of coarctation should use a preparation that mimics the natural lesion.
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PMID:Baroreflex sensitivity and carotid sinus dimensions in dogs with coarctation. 78 71

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.
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PMID:Mechanical and neuro-humoral factors in acute aortic coarctation hypertension. 160 37

To study whether resetting of the baroreceptors is accompanied by normal reflex activity to the heart, we analyzed time-course changes of pressure, heart rate, baroreceptor reflex sensitivity, and plasma renin activity during the development of coarctation hypertension. Baseline heart rate was measured daily, and plasma renin activity and reflex changes in heart rate (bolus injections of either phenylephrine or nitroprusside, 0.2-25.6 micrograms/kg i.v.) were recorded at different times in coarcted and sham-coarcted rats. Hypertension was stable (approximately 39% from baseline mean arterial pressure of 112 +/- 3 mm Hg), whereas heart rate (333 +/- 4 beats per minute) showed a biphasic behavior: bradycardia at 6 hours (264 +/- 7 beats per minute) and tachycardia at 5 days (418 +/- 14 beats per minute). On day 10 of hypertension, heart rate was normal. Plasma renin activity was markedly increased only after 6 hours (4.9 times). Reflex bradycardia exhibited a progressive impairment: The slopes of the regression lines between changes in heart rate and changes in mean arterial pressure were not significantly reduced at 6 and 48 hours when the resetting was in development (changes of 17% and 28% from a control of -1.89 +/- 0.20 beats per minute/mm Hg) but were significantly depressed after the resetting had been completed (-51% and -56% at 5 and 10 days, respectively). Reflex tachycardia was significantly reduced in all periods studied (75%, 78%, 52%, and 61% at 6 hours and 2, 5, and 10 days, respectively; -3.92 +/- 0.42 beats per minute/mm Hg in sham rats).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Feb
PMID:Baroreceptor reflex control of heart rate during development of coarctation hypertension. 173 71

This study determined the influence of pentobarbital anesthesia on the autonomic nervous system control of baroreceptor mediated reflex bradycardia in the rat. Reflex bradycardia was elicited by phenylephrine-induced hypertension in conscious and pentobarbital anesthetized (PA) rats before and after sympathetic blockade with the beta-1 receptor antagonist atenolol or parasympathetic blockade with the peripherally acting muscarinic receptor antagonist methyl-atropine. Reflex bradycardia was significantly decreased by pentobarbital anesthesia. Cardiosympathetic blockade produced equivalent relative decreases in baroreflex gain in conscious and PA rats. In contrast, parasympathetic nervous system blockade with methyl-atropine produced relatively less inhibition of baroreflex gain in the PA rat compared with the conscious rat. These results suggest that pentobarbital anesthesia decreases baroreflex gain by inhibiting vagally mediated reflex bradycardia.
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PMID:The effect of pentobarbital anesthesia on the autonomic nervous system control of heart rate during baroreceptor activation. 176 16

Involvement of the brain renin-angiotensin system in baroreceptor reflex regulation was assessed by recording reflex heart rate and sympathetic nerve responses in normotensive rats that had been infused intracerebroventricularly with the converting enzyme inhibitor enalapril for 15 days. Reflex bradycardia and sympathetic nerve inhibition during pressor responses to phenylephrine were larger in rats with intracerebroventricularly infused enalapril than in control rats similarly infused either intracerebroventricularly with saline or intravenously with enalapril. In contrast, opposite reflex responses to sodium nitroprusside-induced hypotension were mostly unaffected. Because depressor, bradycardic, and sympathoinhibitory responses to electrical stimulation of the central cut end of the left aortic depressor nerve were also enhanced, intracerebroventricularly infused enalapril must be affecting the baroreceptor reflex arc centrally. These results are compatible with the interpretation that intracerebroventricularly infused enalapril enhanced baroreceptor reflex sensitivity by reducing endogenous angiotensin II levels in the brain through converting enzyme inhibition.
Hypertension 1990 Mar
PMID:Baroreceptor reflex enhancement by chronic intracerebroventricular infusion of enalapril in normotensive rats. 230 86

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

Mild hypertension with reduced chronotropic baroreflex sensitivity to phenylephrine occurred in Sprague-Dawley rats fed a high-salt diet for 5 wk. Progressive elevation of systolic and mean pressures, detected initially by indirect tail-cuff measurement, was later verified by direct recording of phasic pressures from indwelling aortic catheters in the same rats. Reflex bradycardia during pressor responses to phenylephrine was consistently less pronounced in salt-loaded than in control rats, whether tested while rats were awake or anesthetized. However, attendant decreases in renal nerve activity were not appreciably altered. Neither central nor carotid baroreceptor mechanisms were considered likely but aortic baroreceptors must have somehow been depressed because increases in afferent aortic nerve activity elicited during intravenous infusion of phenylephrine were invariably smaller in salt-loaded than in control rats. Whatever the underlying mechanisms may be, our results show that when hypertension develops during dietary salt loading, baroreflex chronotropic responses are selectively inhibited while attendant decreases in renal nerve activity are preserved.
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PMID:Dietary salt loading produces baroreflex impairment and mild hypertension in rats. 402 63

The baroreceptor heart rate reflex was studied in 26 renal hypertensive and 17 normotensive rabbits and in 13 rabbits after reversal of hypertension. Blood pressure and heart rate were varied by bolus injections of methoxamine or nitroglycerine in conscious rabbits, and a logistic sigmoid function was fitted to the pressure-heart rate data to estimate upper and lower heart rate plateaus, median blood pressure, and reflex sensitivity. In hypertensive rabbits, resetting of the blood pressure-heart rate curves to higher pressures was associated with reduced reflex sensitivity, increased lower heart rate plateau, and operating pressures significantly greater than the region of maximum reflex sensitivity, resulting in substantial attenuation of reflex bradycardia in response to hypertension. Reflex bradycardia after smoke inhalation was normal. Reversing the hypertension completely reversed the abnormalities in baroreflex control of heart rate. Renal hypertension in the rabbit produces functional changes that are completely reversible in the baroreceptor-heart rate reflex, probably in the afferent limb.
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PMID:Baroreceptor heart rate reflex in rabbits after reversal of renal hypertension. 623 15

Basal heart rate (HR) of conscious rats under resting conditions was measured daily by electrocardiogram (ECG) during the development of one-kidney, one clip (1K1C) hypertension. A progressive increase in HR (mean +/- SEM) was observed from Day 1 to 7: 318 +/- 11; 330 +/- 18, 338 +/- 18; 344 +/- 19; 372 +/- 14; 374 +/- 11, and 388 +/- 12 bpm, respectively. During the same period, mean arterial pressure (MAP) also increase progressively: 126 +/- 2; 129 +/- 2; 134 +/- 4; 135 +/- 7; 144 +/- 2 and 157 +/- 4 mm Hg, respectively. From Day 7 onward, the HR declined, reaching values of 336 +/- 13 bpm on Day 9, with no further alterations for the next 21 days. The MAP continued to rise, however, being 158 +/- 4 on Day 8 and 175 +/- 7 mm Hg on Day 30. Sham-operated rats showed no changes in HR or MAP. During the development of hypertension, blockade of converting enzyme with captopril (10 mg/kg, i.v.) caused a significant blood pressure fall on Day 1 (-27 +/- 1 mm Hg) and Day 3 (-18 +/- 2 mm Hg), whereas on Day 6 (-9 +/- 3 mm Hg) and Day 14 (-8 +/- 3 mm Hg) the fall was not different from that of the normotensive control rats (NCR) (-6 +/- 1 mm Hg). Reflex bradycardia, produced by increasing doses of phenylephrine which elevated the MAP by 10 to 40 mm Hg, was studied in conscious NCR and renal hypertensive rats (RHR) 3 and 7 days after surgery during the development of renal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Tachycardic responses during the development of renal hypertension. 665 59

These experiments were intended to elucidate the role of central mechanisms in the maintenance of high blood pressure produced by deoxycorticosterone (DOC) and salt in rats. We investigated the central effect of angiotensin (AII) on systemic arterial blood pressure and plasma arginine vasopressin (AVP) in DOC-salt and control rats. There was a pronounced augmentation of the pressor responsiveness to centrally injected AII in DOC-salt hypertensive rats; but there was no difference in AII induced AVP release in DOC-salt hypertensive rats compared to sham controls. The increase in vascular resistance of the perfused hindquarters induced by stimulation of the lumbar sympathetic chains did not change in DOC-salt hypertensive rats although the increases induced by norepinephrine (NE) were potentiated at the higher doses. Pressor responsiveness of the DOC-salt hypertensive rats to i.v. administration of AII, AVP and NE was shown to be augmented by factors of 3.6, 2.5 and 1.8 respectively in DOC-salt rats. Reflex bradycardia to these pressor responses was attenuated indicating impairment of baroreflex function. The potentiation of pressor responses to centrally injected AII in DOC-salt hypertensive rats was greater than could be explained by augmented pressor responsiveness to iv NE and AVP. Neither baroreflex dysfunction, facilitated release of NE at sympathetic terminals, nor augmented release of AVP into the circulation could explain the potentiation. Therefore, our data suggested that selective central amplification of sympathetic vasomotor responses to centrally injected AII stimuli may play a role in the hypertension after 3 weeks of DOC-salt treatment in rats.
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PMID:Central mechanisms in DOC-salt hypertensive rats. 711 68


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