Cardiovascular Effects of Prazosin in Dogs

1976 ◽  
Vol 51 (s3) ◽  
pp. 609s-612s ◽  
Author(s):  
I. Cavero
Keyword(s):  
Vascular Tone ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Acute Administration ◽  
Experimental Conditions ◽  
Bilateral Carotid Occlusion ◽  
Pressor Responses ◽  
Bilateral Carotid ◽  
Aortic Blood Pressure ◽  
Stimulation Of

1. In pentobarbitone-anaesthetized dogs, prazosin (2×1·3 μmol day—1 kg—1; 2×0·5 mg day—1 kg—1) administered orally for 3 days reduced resting aortic blood pressure as well as the pressor response to bilateral carotid occlusion. Prazosin neither affected resting heart rate nor the tachycardia induced by intravenous isoprenaline, noradrenaline and electrical stimulation of preganglionic and postganglionic sympathetic nerve fibres. Prazosin significantly attenuated the fall in perfusion pressure in a perfused hind leg resulting from the section of the ipsilateral sympathetic lumbar chain. Furthermore, the drug inhibited by about 50% the hind-leg pressor responses elicited by intra-arterial administration of α-adrenoreceptor agonists and by stimulation of the lumbar sympathetic chain, without altering the effects of angiotensin II. 2. Acute administration of prazosin into the innervated hind leg provoked a dose-related reduction in vascular resistance. However, after spinal anaesthesia no such an effect was observed even when vascular tone was increased by infusion of vasopressin. Under the same experimental conditions administration of papaverine induced a vasodilatation. 3. This study confirms that prazosin impairs the function of vascular α-adrenoreceptors, and strongly challenges the claim that this compound produces a directly mediated vasodilatation of the leg vascular bed.

Cardiovascular effects of homologous bradykinin in rainbow trout

1997 ◽  
Vol 272 (4) ◽  
pp. R1112-R1120 ◽  
Author(s):  
K. R. Olson ◽  
D. J. Conklin ◽  
L. Weaver ◽  
D. W. Duff ◽  
C. A. Herman ◽  
...  
Keyword(s):  
Pressor Response ◽  
Phase 1 ◽  
Venous Pressure ◽  
Cardiovascular Effects ◽  
Phase 2 ◽  
Phase 3 ◽  
Alpha Adrenoceptors ◽  
Pressor Responses ◽  
Stimulation Of

Bradykinins have only recently been identified in fish, and a detailed analysis of their cardiovascular actions is lacking. The present study examines the cardiovascular effects of trout bradykinin ([Arg0,Trp5,Leu8]bradykinin; tBK) in conscious trout, Oncorhynchus mykiss. tBK (1-10 nmol/kg body wt bolus) produced triphasic pressor-depressor-pressor responses. In phase 1, cardiac output (CO), ventral aortic (P(VA)), dorsal aortic (P(DA)), and central venous pressure increased, whereas systemic (R(S)) and gill resistance (R(G)) were unchanged. In phase 2, R(G) increased, whereas R(S), CO, and heart rate decreased, reducing P(VA) and P(DA). Plasma prostaglandin E2 and the prostacyclin metabolite, 6-ketoprostaglandin F1alpha, were significantly elevated during phase 2, whereas leukotrienes C4 and B4 and thromboxane B2 were unaffected. Phase 3 was produced by an increased CO and R(S) and the return of R(G) to control. Phase 1 pressor response was not blocked by inhibitors of cyclooxygenase, angiotensin-converting enzyme (ACE) or alpha-adrenoceptors (alpha-AD), whereas phase 2 depressor and plasma prostaglandin responses were prevented by cyclooxygenase inhibition. Phase 3 was partially blocked by ACE and alpha-AD inhibitors and is a response to the preceding hypotension. In vitro, tBK only decreased vascular resistance in the perfused splanchnic or skeletal muscle-kidney preparations. These results show that although tBK has multiple effects on the trout cardiovascular system, none of the effects are due to direct tBK stimulation of vascular smooth muscle. Phase 2 vasodilation has features consistent with release of vasodilator prostaglandins while the mechanism of phase 1 constriction is unknown.

Central neural regulation of carotid baroreceptor reflexes in the cat

1965 ◽  
Vol 209 (6) ◽  
pp. 1267-1277 ◽  
Author(s):  
Donald J. Reis ◽  
Michel Cuenod
Keyword(s):  
Carotid Sinus ◽  
Pressor Response ◽  
Brain Structures ◽  
Carotid Occlusion ◽  
Carotid Baroreceptor ◽  
Pressor Responses ◽  
Baroreceptor Reflexes ◽  
Aortic Blood Pressure ◽  
The Mean ◽  
Stimulation Of

Reflex changes of the mean aortic blood pressure (BP) to carotid sinus stretch or carotid occlusion in anesthetized vagotomized cats were observed following ablation or electrical stimulation of brain. Decerebration produced augmentation of the depressor response to sinus stretch, reduction of the pressor response to carotid occlusion, and fall of BP. Subsequent cerebellectomy produced an increase of depressor and pressor responses. Midpontine section produced disappearance of the pressor response to carotid occlusion and appearance of a "paradoxical" pressor response to sinus stretch. Stimulation within hypothalamus and reticular formation produced augmentation and a barbiturate-sensitive poststimulus depression of pressor response without changes in BP. It is concluded that baroreceptor reflex responsiveness is under tonic and phasic control of brain structures above medulla and that pressor and depressor limbs of the reflex are not reciprocal and modified independently of each other and of the BP. This suggests functional separation of brainstem neurons involved in reflex and tonic BP control and that some cerebral regulation of BP is indirectly mediated through vascular reflexes.

Systemic responses to carotid occlusion in the anesthetized rat

1992 ◽  
Vol 72 (4) ◽  
pp. 1247-1254 ◽  
Author(s):  
J. M. Lash ◽  
E. Haase ◽  
A. A. Shoukas
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Carotid Occlusion ◽  
Male Rats ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Common Carotid Artery ◽  
Bilateral Carotid ◽  
Common Carotid Artery Occlusion

We evaluated the effects of four standard anesthetization regimens on the systemic cardiovascular responses to bilateral common carotid artery occlusion in 28 adult male rats. Rats were randomly assigned to anesthesia groups: thiopental sodium (PT; 100 mg/kg ip), alpha-chloralose (CH; 100 mg/kg iv), ketamine hydrochloride plus acepromazine (KA; 135 mg/kg and 1.5 mg/kg sc), and pentobarbital sodium (PB; 50 mg/kg ip). PT and PB animals had similar baseline heart rates (HR; 333 and 345 beats/min, respectively) and arterial pressures (MAP; 126 and 118 mmHg, respectively), whereas both were lower in CH and KA (314 and 288 beats/min, 92 and 85 mmHg). During bilateral carotid occlusion, PT demonstrated the largest change in MAP (dMAP; +27 mmHg) but the smallest change in HR (dHR; +8 beats/min). CH and PB demonstrated similar dHR (+24 and +16 beats/min) and dMAP (+20 and +19 mmHg). KA demonstrated a significant dHR (+14 beats/min), but the average dMAP was not statistically significant (+3 mmHg). Therefore, carotid occlusion in rats anesthetized with PT, PB, or CH consistently elicits a systemic arterial pressor response comparable with that reported for conscious animals. When the magnitude and stability of baseline HR and MAP are also considered, PT and PB anesthetization seem to be the most reliable for evaluation of the carotid occlusion pressor response in rats.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

Adrenomedullary pressor responses to stimulation of the rostral hypothalamus in the rat: influence of adrenaline-induced vasodilation and reflex cardioinhibition

1988 ◽  
Vol 66 (2) ◽  
pp. 213-221
Author(s):  
Pierre Gauthier
Keyword(s):  
Pressor Response ◽  
Primary Phase ◽  
Anterior Hypothalamus ◽  
Plasma Noradrenaline ◽  
Current Response ◽  
Adrenergic Blockade ◽  
Hypothalamic Region ◽  
Pressor Responses ◽  
Noradrenaline And Adrenaline ◽  
Stimulation Of

Electrical stimulation (100 Hz, 1 ms, 150 μA, 10 s) of the anterior hypothalamus in chloralose-anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in arterial pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response was accompanied by an increase in plasma noradrenaline and adrenaline levels. Peripheral sympathectomy with guanethidine selectively abolished the primary phase of the biphasic pressor response, while bilateral removal of the adrenal medulla eliminated only the secondary component. After α-adrenergic blockade with phentolamine, the primary phase of the stimulation-induced response was reduced while the secondary pressor component was blocked and replaced by a significant hypotension. The intravenous administration of sotalol enhanced the secondary pressor component without affecting the stimulation-induced plasma noradrenaline and adrenaline responses. After treatment with atropine, the secondary pressor effect was also potentiated, as the reflex bradycardia normally associated with the response was eliminated. A subsequent administration of sotalol in these rats further potentiated the secondary pressor component to stimulation. In rats treated with atropine and sotalol, the sympathetic vasomotor and the adrenomedullary pressor responses could be dissociated according to thresholds and stimulus frequency or current–response characteristics. The results suggest that in intact rats, adrenaline-induced vasodilation and reflex cardiac inhibition contribute to either reduce or mask the adrenomedullary component of the biphasic pressor response evoked by stimulation of the anterior hypothalamus. The study also raises the hypothesis of a dual regulation of both components of the sympathetic system in the anterior hypothalamic region.

A comparison of the effects of acute verses chronic administration of phenoxybenzamine on pressor responses elicited by the selective α1-adrenoceptor agonist cirazoline in the pithed rat preparation

1992 ◽  
Vol 70 (6) ◽  
pp. 916-921 ◽  
Author(s):  
Reza Tabrizchi ◽  
Christopher R. Triggle
Keyword(s):  
Pressor Response ◽  
Chronic Administration ◽  
Inhibitory Effect ◽  
Acute Administration ◽  
Dependent Manner ◽  
Pithed Rat ◽  
Inhibitory Effects ◽  
Receptor Reserve ◽  
Pressor Responses ◽  
The Right

The effects of nifedipine on the pressor responses to cirazoline were examined in the pithed rat preparation that had received either acute or chronic phenoxybenzamine treatment. Phenoxybenzamine was administered, i.v., to conscious rats, either acutely at 0.01, 0.03, and 0.1 mg/kg, 60 min prior to the commencement of the experiments or chronically at 0.1, 0.3, and 1.0 mg/kg, once daily for 7 days. Nifedipine was administered i.a. (1.0 mg/kg) after the animals had been pithed. The acute or chronic administration of phenoxybenzamine alone displaced the dose–response curve to cirazoline to the right in a dose-dependent manner, while reducing the slope function and maximum response to the agonist. The combined effects of acute phenoxybenzamine and nifedipine produced an additive inhibitory effect on the pressor response elicited by cirazoline, which was most apparent following the removal of receptor reserve by acute phenoxybenzamine. The inhibitory effects of nifedipine and chronically administered phenoxybenzamine were additive at the lower administered doses of the alkylating agent but, in contrast with the effects of acute phenoxybenzamine, the enhanced inhibitory effects of nifedipine were reduced following the removal of receptor reserve. These results indicate that the chronic administration of phenoxybenzamine reduces the additive inhibitory effects of nifedipine and phenoxybenzamine that were observed following the acute administration of phenoxybenzamine.Key words: α1-adrenoceptors, vasoconstriction, subtypes, pithed rat, calcium channel antagonist.

The Role of Endogenous Opiates in the Area Postrema Pressor Pathway

1980 ◽  
Vol 59 (s6) ◽  
pp. 267s-269s ◽  
Author(s):  
Julianna E. Szilagyi ◽  
C. M. Ferrario
Keyword(s):  
Angiotensin Ii ◽  
Vertebral Artery ◽  
Area Postrema ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Endogenous Opiates ◽  
Pressor Responses ◽  
Vasomotor Activity ◽  
The Brain

1. Intra-vertebral artery-administered angiotensin II acts at the area postrema to facilitate central sympathetic vasomotor activity. Recent evidence suggests a possible role of the opiate system in the mechanism of action of angiotensin II at the level of the brain stem. 2. In these experiments, we show that the morphine antagonist naloxone reduces significantly the magnitude of the pressor response to vertebral artery-infused angiotensin II. 3. Morphine, in contrast, doubled the peak of the vertebral response to identical doses of the peptide. Neither naloxone nor morphine affected the pressor responses to intravenously administered angiotensin II. 4. The data suggest that the endogenous opiate system in the medulla modulates the cardiovascular effects of angiotensin II at the level of the area postrema.

Pressor response from rostral dorsomedial medulla is mediated by excitatory amino acid receptors in rostral VLM

1994 ◽  
Vol 267 (1) ◽  
pp. R309-R315 ◽  
Author(s):  
Y. Hirooka ◽  
J. W. Polson ◽  
R. A. Dampney
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Amino Acid Receptors ◽  
Control Value ◽  
Afferent Fibers ◽  
Pressor Responses ◽  
Before And After ◽  
Stimulation Of

Excitatory amino acid (EAA) receptors in the rostral part of the ventrolateral medulla (VLM) have been shown to mediate pressor responses elicited by stimulation of various peripheral afferent fibers as well as other central nuclei. This study tested the hypothesis that these receptors are a critical component in the central pathway mediating the powerful pressor response that is produced by stimulation of a group of neurons within a circumscribed region in the rostral dorsomedial medulla (RDM). In anesthetized rabbits, the pressor response elicited by unilateral microinjection of glutamate into this RDM region was measured before and after injection of kynurenic acid (Kyn), a broad-spectrum EAA receptor antagonist, into the physiologically identified pressor region of either the ipsilateral or contralateral rostral VLM. The pressor response to RDM stimulation was greatly reduced (to 24 +/- 4% of control) 5-10 min after injection of Kyn (but not the vehicle solution) into the ipsilateral rostral VLM; this response returned completely to its control value within 30-60 min after Kyn injection. By contrast, after Kyn injection into the contralateral rostral VLM, the pressor response to RDM stimulation was not affected (106 +/- 15% of control). The results indicate that the descending pressor pathway from the RDM to the spinal cord is mediated by EAA receptors in the rostral VLM pressor region. Furthermore, the pathway from the RDM to the rostral VLM is predominantly, if not exclusively, ipsilateral.

Cardiovascular effects of posterior hypothalamic stimulation in baroreflex-denervated rats

1990 ◽  
Vol 259 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
K. W. Barron ◽  
C. M. Heesch
Keyword(s):  
Electrical Stimulation ◽  
Vascular Resistance ◽  
Cardiovascular Effects ◽  
Posterior Hypothalamus ◽  
Intact Group ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Mesenteric Vascular Resistance ◽  
Posterior Hypothalamic Stimulation ◽  
Stimulation Of

The overall purpose of this study was to examine the effect of sinoaortic baroreceptor denervation (SAD) on the cardiovascular and sympathetic outflow responses to electrical stimulation of the posterior hypothalamus. In anesthetized rats that had undergone SAD 7-10 days before experimentation, electrical stimulation of the posterior hypothalamus elicited greater increases in mean arterial pressure, iliac vascular resistance, mesenteric vascular resistance, and lumbar sympathetic nerve activity than in sham-operated baroreceptor-intact animals. Similarly, the pressor effects of intravenous norepinephrine were also augmented in the baroreceptor-denervated group compared with the baroreceptor-intact group. When posterior hypothalamic and intravenous norepinephrine pressor stimuli, which produced equivalent pressor responses in sham-operated baroreceptor-intact animals, were compared in baroreceptor-denervated animals, the pressor effects of the central hypothalamic stimulus were enhanced to a greater degree than the norepinephrine pressor effects. These data provide evidence that arterial baroreceptor reflexes exert greater buffering of pressor stimuli initiated from the central nervous system compared with pressor responses due to peripheral vascular vasoconstrictor agents.

scholarly journals Vestibular stimulation leads to distinct hemodynamic patterning

2000 ◽  
Vol 279 (1) ◽  
pp. R118-R125 ◽  
Author(s):  
I. A. Kerman ◽  
B. A. Emanuel ◽  
B. J. Yates
Keyword(s):  
Vascular Tone ◽  
Systemic Blood Pressure ◽  
Vestibular Stimulation ◽  
Doppler Flowmetry ◽  
Afferent Activation ◽  
Pressor Responses ◽  
Renal Vascular ◽  
Vestibulosympathetic Reflexes ◽  
Renal Vascular Tone ◽  
Stimulation Of

Previous studies demonstrated that responses of a particular sympathetic nerve to vestibular stimulation depend on the type of tissue the nerve innervates as well as its anatomic location. In the present study, we sought to determine whether such precise patterning of vestibulosympathetic reflexes could lead to specific hemodynamic alterations in response to vestibular afferent activation. We simultaneously measured changes in systemic blood pressure and blood flow (with the use of Doppler flowmetry) to the hindlimb (femoral artery), forelimb (brachial artery), and kidney (renal artery) in chloralose-urethane-anesthetized, baroreceptor-denervated cats. Electrical vestibular stimulation led to depressor responses, 8 ± 2 mmHg (mean ± SE) in magnitude, that were accompanied by decreases in femoral vasoconstriction (23 ± 4% decrease in vascular resistance or 36 ± 7% increase in vascular conductance) and increases in brachial vascular tone (resistance increase of 10 ± 6% and conductance decrease of 11 ± 4%). Relatively small changes (<5%) in renal vascular tone were observed. In contrast, electrical stimulation of muscle and cutaneous afferents produced pressor responses (20 ± 6 mmHg) that were accompanied by vasoconstriction in all three beds. These data suggest that vestibular inputs lead to a complex pattern of cardiovascular changes that is distinct from that which occurs in response to activation of other types of somatic afferents.

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