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

A cardiogenic hypertensive chemoreflex was studied in 38 anesthetized and three unanesthetized dogs. Serotonin (100 mug/ml) injected into either the left atrium or small brancehes of the proximal left coronary artery produced a maximal response, with 96 +/- 18 mm Hg increment in mean aortic pressure within 6 +/- 2 seconds, lasting about 1 min; a later phase of the same hypertension lasted 9 +/- 5 minutes more and could partially be produced with serotonin injected into the thoracic aorta. Injections into the distal left coronary artery produced only the Bezold-Jarisch reflex. Concomitant with the immediate hypertension there were vagal and sympathetic efferent effects in both the sinus node and the atrioventricular (A-V) junction. Either of these effects could be selectively eliminated and the other augmented by direct local perfusion with an appropriate cholinergic (atropine 10 mug/ml) or adrenergic beta-receptor (propranolol 10 mug/ml) blocking agent. Bilateral vagotomy markedly attenuated but did not eliminate the acute hypertension, but it abolished both chronotropic and dromotropic effects. Phentolamine (2 mg/min i.v.) markedly diminished the hypertensive response. Guanethidine or reserpine pretreatment markedly diminished the hypertensive response; reserpine eliminated the electrophsiologic effects but guanethidine did not. Infiltration of serotonin around the main left coronary partially reproduced the reflex, but similar infiltration of xylocaine hydrochloride blocked the reflex. Serial section histologic studies of the region around the main left coronary atery in seven dog hearts and nine human hearts demonstrated the presence of a small structure resembling a chemoreceptor; its blood supply originated from the left coronary artery. Some possible clinical implications are discussed.
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PMID:Analysis of components in a cardiogenic hypertensive chemoreflex. 114 1

The effects of serotonin (5-hydroxytryptamine; 5-HT) on the cardiovascular system are complex. These effects, consisting of bradycardia or tachycardia, hypotension or hypertension, and vasodilation or vasoconstriction are mediated by three main sets of receptors called 5-HT1-like, 5-HT2, and 5-HT3. In addition, recent findings suggest the participation of a putative 5-HT4 receptor. Though selective 5-HT1A receptor agonists can lower heart rate (and arterial blood pressure), 5-HT usually lowers heart rate by eliciting an initial short-lasting hypotension due to bradycardia (von Bezold-Jarisch-like reflex) via 5-HT3 receptors located on sensory vagal nerve endings in the heart. Once this bradycardia reflex is suppressed--for example, during deep anesthesia, vagotomy, or spinal section--5-HT can increase heart rate in different species by a variety of mechanisms. Myocardial 5-HT1-like, 5-HT2, and 5-HT4 receptors appear to be involved in the cat, rat, and pig, respectively. 5-HT-induced tachycardia in the dog and rabbit is due mainly to release of catecholamines and involves 5-HT2 receptors on the adrenal medulla and 5-HT3 receptors on postganglionic cardiac sympathetic nerve fibers. Recently, 5-HT3 receptors also have been implicated in the 5-HT-induced tachycardia in the conscious dog. The blood pressure response to 5-HT is usually triphasic and consists of a von Bezold-Jarisch-like reflex, a middle pressor phase, and a longer-lasting hypotension. The pressor response is a consequence of vasoconstriction mediated via 5-HT2 receptors; however, vasoconstriction in the dog saphenous vein and cephalic arteries and arteriovenous anastomoses is due to stimulation of 5-HT1-like receptors. The depressor response exclusively involves 5-HT1-like receptors located at four different sites: (a) central nervous system (decrease in sympathetic and increase in vagal nervous activity), (b) sympathetic nerve terminals (reduction of transmitter release), (c) vascular smooth muscle (vasodilatation), and (d) vascular endothelium (release of a relaxant factor, probably nitric oxide). Arteriolar dilatation, together with the constriction of arteriovenous anastomoses, leads to an increase in nutrient (tissue; capillary) blood flow. The 5-HT1-like receptors are heterogeneous in nature; however, apart from the resemblance of the central nervous system 5-HT1-like receptor causing hypotension and bradycardia to the 5-HT1A binding subtype, the relationship of the other 5-HT1-like receptors to 5-HT1 binding subtypes is still debatable.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular effects of serotonin agonists and antagonists. 170 84

In severe preeclampsia, short-term peripartum management of hypertension with hydralazine is complicated by relatively prolonged hypotensive episodes, resulting in fetal distress. We hypothesized that nitroprusside's rapid onset and brief antihypertensive action would permit more controlled blood pressure reduction. Nitroprusside was infused into 10 invasively monitored subjects until mean arterial pressure either 1) was gradually reduced 10-20% or 2) fell abruptly. Subjects fell into two groups, defined by whether the hypotensive effect of nitroprusside was accompanied by a fall in heart rate (group A, n = 8) or a rise (group B, n = 2). Group B showed the expected sinoaortic baroreceptor reflex elevations in heart rate (+17 +/- 6 beats/min) in response to moderate falls in mean arterial pressure (-32 +/- 9 mm Hg) elicited by moderate doses (1.03 +/- 0.23 micrograms/kg/min). However in group A, steep reductions in mean arterial pressure (-75 +/- 22 mm Hg, p less than 0.0001), significantly greater than in group B (p less than 0.05), occurred at much lower doses (0.35 +/- 0.23 micrograms/kg/min; p less than 0.05) and were accompanied by falls in heart rate (-21 +/- 7 beats/min). The apparently paradoxical falls in heart rate and extreme hypotensive responses in group A indicate severe circulatory compromise, corresponding to the cardiac and vasomotor depression that characterizes severe hemorrhage and other forms of acute/severe hypovolemic hypotension. This hemodynamic pattern represents a cardiopulmonary baroreceptor reflex presumably related to the Bezold-Jarisch reflex. The appearance of this pattern in the present study probably reflects the imposition of nitroprusside's prominent venous dilator action on the relatively reduced blood volume that generally characterizes severe preeclampsia.
Hypertension 1991 Jul
PMID:Nitroprusside in preeclampsia. Circulatory distress and paradoxical bradycardia. 186 Jul 15

Quipazine (0.5-2 mg/kg i.v.) produced transient hypotension and bradycardia followed by sustained hypertension and variable effects on heart rate in anaesthetized rats. The hypotension, bradycardia and sympatho-inhibitory effects of quipazine were attenuated by bivagotomy. In bivagotomized rats, the hypertension produced by quipazine was not modified by hexamethonium or prazosin but was abolished by ritanserin (1 mg/kg i.v.). In ritanserin-treated rats, section of the carotid sinus nerves and vagus nerves or ICS 205.930 (0.1 mg/kg i.v.) abolished the hypotensive, bradycardic and sympatho-inhibitory effects of quipazine; the action of quipazine was not reproducible in these rats. Quipazine also inhibited the Bezold-Jarish reflex elicited by 5-HT (20 micrograms/kg i.v.). In ICS 205.930-treated rats, the hypertension evoked by quipazine was associated with a reduction in splanchnic nerve activity due to stimulation of baroreceptors. The renin-angiotensin system is not involved in the hypertensive response. The increase in heart rate produced by quipazine in bivagotomized rats was reduced by ritanserin and tertatolol (0.1 mg/kg i.v.) and abolished by a combination of both drugs. We conclude that the bradycardic and sympatho-inhibitory effects of quipazine result from activation of 5-HT3 receptors located in the cardiopulmonary area and of carotid body chemoreceptors. The hypertension and tachycardia are mediated by vascular and myocardial 5-HT2 receptors. No evidence was obtained for a central sympatho-excitatory effect.
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PMID:The cardiovascular effects of quipazine are mediated by peripheral 5-HT2 and 5-HT3 receptors in anaesthetized rats. 212 77

The cardiovascular effects of 5-hydroxytryptamine (5-HT), consisting of bradycardia or tachycardia, hypotension or hypertension, and vasodilatation or vasoconstriction, are mediated by three main types of receptors called 5-HT1-like, 5-HT2, and 5-HT3. In intact animals 5-HT elicits a short-lasting bradycardia, accompanied by hypotension, via stimulation of 5-HT3 receptors located on sensory vagal nerve endings in the heart (Bezold-Jarisch reflex). The nature of 5-HT receptors mediating tachycardiac responses is species-dependent. Myocardial 5-HT1-like and 5-HT2 receptors subserve tachycardia in the cat and rat, respectively. Tachycardia in the dog and rabbit is due to a release of catecholamines effected via the 5-HT2 receptors on the adrenal medulla and the 5-HT3 receptors on postganglionic cardiac sympathetic nerve fibres, respectively. The receptors mediating tachycardia in the pig are unique as they do not resemble any of the three 5-HT receptors characterized so far. The blood pressure response to 5-HT is usually triphasic: initial short-lasting hypotension due to reflex bradycardia (via 5-HT3 receptors), a middle pressor phase (via 5-HT2 receptors), and a longer-lasting hypotension (via 5-HT1-like receptors). Vascular contraction by 5-HT is generally mediated by 5-HT2 receptors (located primarily on the large conducting vessels), though in some instances (e.g., dog saphenous vein, dog and human basilar artery, and porcine arteriovenous anastomoses) the contractile response is (also) mediated via 5-HT1-like receptors. Venous dilatation and arteriolar dilatation (leading to increased capillary ['nutrient'] blood flow) occur via 5-HT1-like receptors located mainly on the vascular smooth muscles but also on the endothelium; the smooth muscle and endothelial 5-HT1-like receptors seem to be heterogeneous. In addition, 5-HT can elicit vasodilatation and hypotension as a result of decreased sympathetic nervous tone by acting within the central nervous system and by inhibiting noradrenaline release by a presynaptic action. Both these effects also involve 5-HT1-like receptors that do not appear to be identical. Last, knowledge of the cardiovascular effects of 5-HT and the nature of the receptors involved should be helpful in developing 5-HT-related compounds that may be useful in the treatment of hypertension, migraine, and peripheral vascular diseases.
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PMID:Cardiovascular effects from stimulation of 5-hydroxytryptamine receptors. 267 Jul 24

The effect of arginine vasopressin (AVP) on the arterial baroreflex control of heart rate (HR) was studied in intact and sinoaortic-denervated (SAD) conscious, unrestrained monkeys. A baroreflex curve for mean arterial blood pressure (MABP) and HR was determined before and during intravenous infusion of AVP (2-4 mU.kg-1.min-1) and after the AVP vascular antagonist "Manning compound" [( d(CH2)5Tyr(Me)]AVP, 40 micrograms/kg), while AVP infusion was kept running. The sensitivity (slope) of the arterial baroreflex, as well as the reflex bradycardia induced by high blood pressure, increased significantly during AVP and returned to the control level after Manning compound. The effect of AVP on the Bezold-Jarisch reflex (induced by stimulating left ventricular receptors with 4 micrograms/kg veratridine injected in the left atrium) was also studied. The cardiovascular responses to veratridine were examined before and during AVP and after administration of Manning compound together with AVP infusion. AVP significantly potentiated the hypotension and the bradycardia produced by veratridine, whereas Manning compound blunted this potentiation. The ventricular reflex in SAD monkeys was significantly greater than in intact monkeys. We conclude that, in the conscious nonhuman primate, AVP potentiates the sensitivity of the baroreflex control of HR as well as the Bezold-Jarisch reflex. The potentiation of the Bezold-Jarisch reflex by AVP in the SAD animals is consistent with a central action, since the baroreceptors and ventricular receptors both have connections in the nucleus tractus solitarius. However, it does not rule out the possibility of peripheral actions on receptors or end organs.
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PMID:Vasopressin potentiates ventricular and arterial reflexes in the conscious nonhuman primate. 273 28

Effects of brevetoxin were evaluated in cats anesthetized with pentobarbital under conditions of controlled end-expiratory pCO2 and constant body temperature. Recordings were made of arterial blood pressure, heart rate, respiratory pattern, diaphragm EMG, evoked tibialis muscle twitch and evoked contraction of the nictitating membrane. Electrical stimulation was employed for periodic excitation of the medullary respiratory center, the phrenic nerve, the peroneal nerve and the cervical sympathetic nerve. Brevetoxin was prepared at a concentration of 1.0 mg/ml in an aqueous medium of 2.5% ethanol plus 2.5% Emulphor 620 (General Aniline and Film Corp., New York). Small i.v. bolus injections of the toxin (40 micrograms/kg) evoked, without tachyphylaxis, the Bezold-Jarisch reflex triad of bradycardia, hypotension and bradypnea. This effect was essentially abolished by vagotomy. Continued injections then resulted in pressor reactions and tachycardia, along with the development of respiratory dysrhythmia. Large doses of brevetoxin (160 micrograms/kg i.v.) caused somatomotor seizures accompanied by severe hypertension, that occurred even after decerebration and cervical spinal cord transection. Cranial intra-arterial and intra-cerebroventricular injections of brevetoxin produced hypertension and respiratory depression more effectively than did i.v. injections. Systemic cumulation of the toxin, with the respiration supported artificially, caused death from cardiovascular collapse, without significant blockade of neuromuscular and ganglionic transmission. It is concluded that brevetoxin exerts its major toxic effects on the circulation and respiration through reflex and central actions, largely sparing peripheral motor mechanisms.
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PMID:Neurological analysis of respiratory, cardiovascular and neuromuscular effects of brevetoxin in cats. 299 23

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

Cardiovascular responses to intravenous bolus doses of certain exogenous substances (capsaicin, phenyldiguanide, cryptenamine, veratrine sulphate) which act on chemoreceptors in the pulmonary or proximal arterial circulation were compared to the naturally occurring chemoreceptor agonist, leucineenkephalin (Leu5-ENK) in the conscious dog. Capsaicin (40 micrograms/kg) and phenyldiguanide (40 micrograms/kg) produced hypotension and bradycardia 5 to 12 sec after injection (P less than 0.05) followed by hypertension (P less than 0.05). Cryptenamine (5 micrograms/kg) produced only hypotension and bradycardia (P less than 0.05) whereas Leu5-ENK (35 micrograms/kg) produced only hypertension and tachycardia (P less than 0.05). The hypotension and bradycardia produced by capsaicin and phenyldiguanide occurred earlier than the pressor response to Leu5-ENK, capsaicin, and phenyldiguanide and the depressor response to veratrine (P less than 0.05). Cryptenamine (5 micrograms/kg) and Leu5-ENK (35 micrograms/kg) when given together had additive effects on heart rate but interacted significantly in influencing blood pressure (P less than 0.05). It is concluded that the early response to capsaicin and phenyldiguanide are compatible with stimulation of known pulmonary chemoreceptors (including J receptors) whereas the pressor effect of phenyldiguanide and Leu5-ENK and the depressor response to veratrum alkaloids are due to activation of receptors in the proximal arterial circulation. The influence of Leu5-ENK on the haemodynamic response to veratrine suggest that ENK may modulate the Bezold-Jarisch reflex.
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PMID:Comparative cardiovascular responses to intravenous capsaicin, phenyldiguanide, veratrum alkaloids and enkephalins in the conscious dog. 395 49

1 In cats anaesthetized with pentobarbitone, observations were made on respiration, spontaneous and evoked diaphragmatic electromyograms, blood pressure, heart rate, indirectly-induced contractions of the anterior tibialis muscle and nictitating membrane, and electrical excitability of the inspiratory centre in the medulla oblongata.2Gymnodinium breve toxin (GBTX) was administered intravenously, intra-arterially to the brain, and intracerebroventricularly. Physiological effects were recorded while alveolar P(CO) (2) was controlled at a constant level except when changes in gas tension were made in order to measure CO(2)-ventilatory responsiveness.3 Adequate doses of GBTX given intravenously by bolus injection elicited a non-tachyphylactic reflex response triad of apnoea, hypotension and bradycardia mediated by the vagus nerves independently of arterial baroreceptor and chemoreceptor innervation.4 After vagotomy, additional amounts of GBTX (i.v.) resulted in apneustic breathing, hypertension and tachycardia. The cardiovascular effects were abolished by ganglionic blockade with hexamethonium.5 Smaller doses of GBTX were required intra-arterially and intracerebroventricularly than by the intravenous route of injection to produce respiratory irregularity and cardiovascular hyperactivity.6 Evoked motor responses, electrical excitability of the medulla oblongata and CO(2)-ventilatory responsiveness were largely spared even though GBTX caused marked disturbances in respiratory rhythmicity and cardiovascular functions.7 It is concluded that GBTX acts reflexly on vagally innervated receptors to evoke a Bezold-Jarisch effect but that the toxin further acts centrally to cause irregular breathholding and hypertension with tachycardia, leading ultimately to respiratory and circulatory failure.
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PMID:Central respiratory and circulatory effects of Gymnodinium breve toxin in anaesthetized cats. 719 40


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