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

This study investigated norepinephrine release during electrical nerve stimulation and inhibitory characteristics of presynaptic alpha 2-adrenoceptors in perfused mesenteric vasculature from deoxycorticosterone acetate (DOCA)-salt hypertensive rats (7-8 weeks after surgery). Electrical stimulation of sympathetic innervation caused a significantly greater release of endogenous norepinephrine into the mesenteric vasculature of DOCA-salt hypertensive rats than in age-matched normotensive controls. Pressor responses to electrical nerve stimulation were also enhanced in DOCA-salt hypertension. Yohimbine, a potent alpha 2-adrenoceptor blocking agent, potentiated the stimulation-evoked release of norepinephrine into the vasculature in normotensive rats. This effect was blunted in DOCA-salt hypertension. These results suggest that increased norepinephrine release from the sympathetic nerve endings in DOCA-salt hypertension might partly reflect an impaired presynaptic alpha 2-adrenoceptor-mediated inhibition, which could enhance vascular sympathetic tone in this model of hypertension.
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PMID:Inhibition of norepinephrine release by presynaptic alpha 2-adrenoceptors in mesenteric vasculature preparations from chronic DOCA-salt hypertensive rats. 254 35

We explored the urodynamic action of clonidine (preferential alpha 2-agonist) and yohimbine (preferential alpha 2-blocker) in decerebrate cats. These animals retain catecholaminergic fibers from the complex of the locus coeruleus to the spinal cord and have synergic and faster micturition cycles than normal cats. Twenty-nine male cats were made decerebrate at intercollicular level under ether anesthesia. Voiding, vesical, urethral and blood pressures, and the EMG of the external sphincter-pelvic floor and leg muscles were studied. Preparations with the urethrovesical junction opened and closed were used. Control activity was characterized by two types of vesical pressure waves: (1) low frequency, high intensity, and (2) high frequency, low intensity. Type-2 preceded Type-1 waves. Clonidine caused: (A) reduction of Type-1 and enhancement of Type-2 Pves waves; (B) diminution of vesical capacity; (C) facilitation of external sphincter relaxation; (D) inhibition of skeletal muscle activity; (E) systemic hypotension and bradycardia. Yohimbine inhibited clonidine's actions. When injected alone, it inhibited vesical and increased sphincteric activities. It also produced systemic hypertension and enhanced crisis of autonomic dysreflexia. The overall effect of clonidine on urodynamics in acute decerebrate cats was to bring about an active, small (normotonic) bladder with urinary frequencies. We suggest that clonidine: (1) inhibited Type-1 waves by inhibiting cellular activity in the locus coeruleus. As a result, the vesico-vesical contraction long loop reflex was abolished; (2) facilitated Type-2 waves by inhibiting inhibitory interneurons in the sacral parasympathetic center. As a result, the vesicovesical contraction short loop reflex was facilitated.
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PMID:Action of clonidine on micturitional reflexes in decerebrate cats. 256 9

Xylazole (Xyl) is an analogue of xylazine (Xyn) synthesized by Lanzhou Institute of Chinese Traditional Veterinary Medicine. The effects of Xyl on heart rate and blood pressure were studied in 5 conscious dogs. Xyl 1 mg/kg iv was similar to Xyn in producing bradycardia and an initial transient hypertension followed by a lasting hypotension which was less significant than Xyn. Yohimbine (0.1 and 0.3 mg/kg), an alpha 2-adrenoreceptor blocking agent, antagonized bradycardia and hypotension induced by Xyl. Tolazoline (3.3 mg/kg), a nonselective alpha-adrenoreceptor blocking agent, reversed the bradycardia and hypotensive effect. Prazosin (1 mg/kg), an alpha 1-adrenoreceptor blocking agent, did not change Xyl-induced bradycardia and hypotension. Atropine (20 micrograms/kg) not only antagonized Xyl-induced bradycardia but also changed from bradycardia to tachycardia, and greatly potentiated Xyl-induced hypertension for more than 30 min. The results suggested that Xyl-induced cardiovascular effects are similar to Xyn that mediated by alpha 2-adrenoreceptor.
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PMID:[Effects of xylazole on heart rate and blood pressure in conscious dogs]. 257 38

The effects of jingsongling (JSL) and xylazine on heart rate (HR) and mean arterial pressure (MAP) were studied in five conscious male dogs. An i.v. injection of xylazine (1 mg/kg) caused a bradycardia, an initial hypertension, and a subsequent hypotension. An i.v. injection of JSL (1 mg/kg) caused a bradycardia and a 20-min hypertension without a subsequent hypotension. Atropine sulfate (45 micrograms/kg, i.v.) increased HR for 30 min without changing MAP, and antagonized JSL-induced bradycardia for at least 60 min. There was a subsequent rebound bradycardia. Atropine sulfate potentiated JSL-induced hypertension in both magnitude and duration. Yohimbine (0.1 mg/kg, i.v.), an alpha 2-adrenoceptor antagonist, increased HR and MAP for 110 and 70 min, respectively. Yohimbine not only failed to potentiate but even reversed the pressor effect of JSL in a dose-dependent manner. Yohimbine also caused a dose-dependent reversal of JSL-induced bradycardia. Tolazoline (5 mg/kg, i.v.), a nonselective alpha-adrenoceptor antagonist, increased MAP for 20 min without changing HR. Tolazoline also reversed JSL-induced hypertension and bradycardia. Prazosin (1 mg/kg), an alpha 1-adrenoceptor antagonist, decreased MAP and increased HR for at least 110 min. Prazosin reversed JSL-induced hypertension but failed to affect JSL-induced bradycardia. These results indicated that: (1) JSL-induced bradycardia and hypertension are mediated by alpha 2-adrenoceptors; (2) yohimbine and tolazoline may be useful in antagonizing these untoward reactions associated with JSL administration, whereas prazosin and atropine were not found to be beneficial in this regard.
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PMID:The effects of jingsongling, a xylazine analog, on mean arterial blood pressure and heart rate in dogs--influences of yohimbine, tolazoline, prazosin, and atropine. 281 Apr 77

The effects of xylazine on heart rate (HR) and mean arterial blood pressure (ABP) were studied in 5 conscious male dogs. An IV injection of xylazine (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia. Xylazine administration also caused an initial increase in ABP, which was followed by a decrease. Atropine sulfate (0.045 mg/kg, IM) increased both the ABP and HR, but prevented xylazine-induced bradycardia only in 3 of 5 dogs. The other 2 dogs had to be given a supplemental dose of atropine sulfate (0.01 mg/kg, IV) before xylazine-induced bradycardia was antagonized. In addition, atropine sulfate potentiated xylazine-induced hypertension for 60 minutes. Yohimbine, an alpha 2-adrenoreceptor blocking agent, given IV at a dosage of 0.1 mg/kg, antagonized hypertension, hypotension, and bradycardia induced by xylazine. In addition, doxapram HCl, given IV at a dosage of 5.5 mg/kg, antagonized bradycardia but potentiated xylazine-induced hypertension, and an IV injection of 4-aminopyridine at a dosage of 0.5 mg/kg did not affect the cardiovascular actions of xylazine. It was concluded that atropine sulfate at the IM dosage of 0.045 mg/kg may be insufficient to antagonize xylazine-induced bradycardia but may potentiate xylazine-induced hypertension, and yohimbine may be useful in antagonizing these untoward reactions associated with xylazine administration. Doxapram and 4-aminopyridine were not found to be beneficial.
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PMID:Effect of xylazine on heart rate and arterial blood pressure in conscious dogs, as influenced by atropine, 4-aminopyridine, doxapram, and yohimbine. 285 5

Chronic (3-day) treatment with prazosin causes an increase in renal alpha 2-adrenergic receptor density and the relocation of renal tubular alpha 2-adrenergic receptors from extrajunctional to postjunctional sites. We investigated whether chronic prazosin treatment (2 mg/kg, i.p.) caused a functional alteration of other renal alpha 2-adrenergic receptors, using the isolated perfused rat kidney. Prazosin significantly reduced blood pressure and increased heart rate during the 3-day treatment. Renal nerve stimulation (2-8 Hz, 10 V, 1 msec) caused a frequency-dependent increase in renovascular resistance, which was potently blocked by prazosin in vitro in both control and prazosin-treated rat kidneys. The vasoconstrictor response to the alpha 2-adrenergic receptor-selective agonist BHT 933 (3-300 microM) was significantly higher in kidneys from prazosin-treated rats. Yohimbine (3-300 nM) potentiated the response to renal nerve stimulation in both treatment groups. The increase in vascular resistance following renal nerve stimulation was lower in kidneys from prazosin-treated rats, but the response to the alpha 1-adrenergic receptor agonist methoxamine (0.3-1 microM) was unchanged. Further studies revealed that renal nerve stimulation-evoked norepinephrine release from prazosin-treated rat kidneys was significantly lower than release from untreated controls. This response could be normalized to control levels by a combination of cocaine (10 microM) and yohimbine (100 nM). Thus, chronic prazosin treatment caused enhanced alpha 2-adrenergic receptor-mediated vasoconstriction and facilitated renal prejunctional inhibitory mechanisms. We conclude that with chronic alpha 1 adrenergic receptor blockade there is increased alpha 2-adrenergic receptor function in at least two and possibly three sites in the kidney; these include postjunctional tubular, prejunctional vascular, and possibly extra-junctional vascular sites.
Hypertension 1987 Jun
PMID:Prazosin-induced alterations in renal alpha-adrenergic receptor function. 288 71

Since it is not known for certain which alpha-adrenergic receptors mediate renal vasoconstriction in human essential hypertension, we infused either doxazosin (n = 7) or yohimbine (n = 7) into the renal arteries of hypertensive subjects immediately prior to diagnostic angiography. Both agents caused an increment in renal blood flow as assessed with the xenon-washout technique. Doxazosin increased renal flow from 342 +/- 36 to 360 +/- 55 ml/min per 100 g (0.05 less than p less than 0.10). Yohimbine enhanced flow from 380 +/- 41 to 485 +/- 63 ml/min per 100 g (p less than 0.01). The effect of yohimbine was significantly greater than that of doxazosin. In a control group (n = 7) receiving only saline, no changes in renal blood flow occurred. Doxazosin enhanced renin secretion in the kidney by 10 +/- 4% over levels in controls (0.05 less than p less than 0.10), whereas yohimbine increased renin release by 80 +/- 23% (p less than 0.01). The latter increase was apparently not due to alterations in flow alone, since the arteriovenous gradient for renin also widened. We conclude that in resting conditions, neurogenic vascular tone in the kidney depends mainly upon activation of alpha 2-adrenergic receptors. Moreover, these receptors exert a tonic inhibitory influence on renin release.
Hypertension 1987 Jun
PMID:Role of alpha 1- and alpha 2-adrenergic receptors in the human hypertensive kidney. 288 75

The role of alpha 2-adrenergic receptor stimulation in the regulation of systemic vascular capacity and venous return, a major determinant of cardiac output, is not well understood. With the influence of the central nervous system isolated from the systemic circulation, the direct peripheral vascular effects of two specific, chemically distinct alpha 2-adrenergic receptor agonists, UK 14,304 and B-HT 920, were investigated in 19 dogs on total cardiopulmonary bypass with constant arterial perfusion and central venous pressure. Five-minute intra-arterial infusions of UK 14,304 (200 micrograms/min) resulted in increased arterial resistance (mean arterial pressure increased 18 +/- 4 [SEM] mm Hg; p less than 0.01) and a decrease in systemic vascular capacity (81 +/- 20 ml; p less than 0.01). This decrease in systemic vascular capacity appears to result from vasoconstriction, since there was no decrease in transhepatic resistance to portal flow and no significant change in hepatic vein flow to suggest redistribution of arterial blood flow. Yohimbine abolished both the arterial and systemic capacity effects, whereas prazosin did not. Intra-arterial administration of B-HT 920 (200 theta grams/min) in five dogs produced similar changes in arterial resistance and systemic capacity. These findings provide direct evidence for beta 2-adrenergic control, not only of arterial resistance but also of systemic vascular capacity, which in the intact animal would increase venous return to the heart.
Hypertension 1988 Apr
PMID:Direct effects of alpha 2-adrenergic receptor stimulation on intravascular systemic capacity in the dog. 289 36

The effect of amitraz on heart rate (HR) and mean aortic blood pressure (MAP) were studied in five conscious male dogs. An iv injection of amitraz (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia for at least 60 min. Administration of amitraz also caused an increase in MAP for 20 min. Atropine sulfate (0.045 mg/kg, iv) increased HR and prevented amitraz-induced bradycardia. In addition, atropine potentiated amitraz-induced hypertension for 45 min. Yohimbine, an alpha 2-adrenoreceptor antagonist, given iv at 0.1 mg/kg, prevented hypertension, bradycardia, and sinus arrhythmia induced by amitraz. Tolazoline, a nonselective alpha-adrenoreceptor antagonist, given iv at 5 mg/kg, reduced the bradycardia and sinus arrhythmia caused by amitraz administration but did not change amitraz-induced hypertension. Tolazoline alone also increased both HR and MAP. Prazosin, an alpha 1-adrenoreceptor antagonist, given iv at 1 mg/kg, did not affect the cardiovascular actions of amitraz. The results suggest that (1) alpha 2-adrenoreceptors mediate amitraz-induced bradycardia and hypertension, and (2) yohimbine, but not atropine, can be used to control the untoward reactions of amitraz.
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PMID:Effect of amitraz on heart rate and aortic blood pressure in conscious dogs: influence of atropine, prazosin, tolazoline, and yohimbine. 301 23

The present study was designed to evaluate the role of the presynaptic alpha 2-adrenoceptor in the pathogenesis of hypertension. Norepinephrine overflow during sympathetic nerve stimulation and its changes by presynaptic alpha 2-adrenoceptor inhibition were examined in the perfused mesenteric vasculatures of young and adult spontaneously hypertensive rats (SHR) compared with age-matched Wistar Kyoto rats (WKY). Electrical sympathetic nerve stimulation caused significantly greater overflow of endogenous norepinephrine from the adrenergic nerve terminals in young SHR than in age-matched WKY. Yohimbine, an alpha 2-adrenoceptor blocking agent, facilitated norepinephrine overflow from the adrenergic nerve terminals. The effects of yohimbine on norepinephrine overflow and pressor responses to electrical nerve stimulation were less in young SHR than in age-matched WKY. Norepinephrine overflow in adult SHR was similar to that in adult WKY, and differences in the effect of yohimbine on norepinephrine overflow between SHR and WKY were not marked at this chronic stage. These results suggest that enhanced norepinephrine overflow in the mesenteric vasculatures can be observed only in young SHR; this may be due in part to an impaired negative feed-back mechanism on the nerve terminals by presynaptic alpha 2-adrenoceptors.
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PMID:Presynaptic alpha 2-adrenoceptor mediated regulation of norepinephrine release in perfused mesenteric vasculatures in young and adult spontaneously hypertensive rats. 303 49


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