Biomedical subjects

R Tabrizchi

Publications and source records attributed to R Tabrizchi.

At least 55 records · Page 3Linked to original sources

PubMed1991

Pressor actions of arginine vasopressin in pithed Sprague-Dawley, Wistar-Kyoto and spontaneously hypertensive rats before and after treatment with nifedipine or pertussis toxin.

The pressor actions of arginine vasopressin (AVP) were examined in pithed Sprague-Dawley and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Prior to pithing, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded via an intra-arterial catheter from sodium pentobarbital anaesthetized rats. SBP and DBP recorded from SHR were significantly greater than those from Sprague-Dawley and WKY rats. However, after pithing, there were no significant differences between DBP among the various strains. Pertussis toxin pretreatment significantly reduced the prepithing SBP and DBP of the SHR but not Sprague-Dawley or WKY rats. Administration of nifedipine significantly reduced DBP of pithed rats. The dose-diastolic pressure response curves obtained from infusion of AVP in Sprague-Dawley and WKY rats were not significantly different from one another, but the maximal vasopressor responses to AVP in pithed SHR were enhanced. Administration of nifedipine to Sprague-Dawley and WKY rats did not affect the dose-response curve to AVP, but nifedipine administration in SHR led to a significant inhibition of the pressor responses to AVP. Furthermore, pertussis toxin pretreatment of rats significantly reduced a component of the AVP pressor effect in SHR but not Sprague-Dawley or WKY rats. We speculate that, in SHR, vasopressin receptors are coupled to a pertussis toxin-sensitive G protein that, in turn, may couple to a dihydropyridine-sensitive calcium channel and also to a pertussis-insensitive G protein that is probably coupled to the phospholipase C/intracellular calcium release process. A component of the elevated blood pressure in SHR is also regulated by a pertussis toxin-sensitive process.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effects of endothelin 3 on diastolic blood pressure of pithed Sprague-Dawley, Wistar Kyoto, and spontaneously hypertensive rats before and after pretreatment with nifedipine.

Pressor actions of endothelin 3 (ET3) were examined in pithed Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive (SH) rats before and after the administration of the calcium channel antagonist, nifedipine. Systolic and diastolic blood pressures were recorded via an intra-arterial catheter from sodium pentobarbital anaesthized rats prior to pithing. The systolic and diastolic blood pressures recorded from SH rats were significantly greater than those of SD and WKY rats; however, after pithing there were no significant differences between the diastolic blood pressures among the various strains. Administration of nifedipine significantly reduced the diastolic blood pressure of pithed rats to an equal extent in all three strains. The infusion of ET3 produced a dose-dependent increase in diastolic blood pressure of SD, WKY, and SH rats, but neither vascular sensitivity nor reactivity to ET3 was altered in SH rats. Nifedipine was more effective at inhibiting the vasoactive actions of ET3 in SD and WKY than in SH rats. It was therefore concluded that the pressor actions of ET3 in SH rats may be less dependent on the influx of calcium through a dihydropyridine-sensitive calcium channel as compared with WKY and SD rats.

Animals↗

PubMed1991

Effects of staurosporine on the pressor responses to alpha-adrenoceptor agonists in pithed rats: a comparison with nifedipine.

The effects of the calcium channel antagonist nifedipine and the protein kinase C (PKC) inhibitor, staurosporine were examined on the pressor actions of a full, cirazoline, and a partial, St587, alpha 1-adrenoceptor agonist as well as the alpha 2-adrenoceptor agonist B-HT 920 in the pithed rat preparation. Administration of nifedipine or staurosporine significantly reduced the diastolic blood pressure of pithed rats. Staurosporine displaced the dose-diastolic pressure response curves for B-HT 920 and St587 to the right in a dose-dependent manner. The ED50 value for the dose-response curves to B-HT 920 and St587 were found to be significantly increased after the administration of staurosporine. Staurosporine also caused a depression of the maximum response to B-HT 920 and St587. The presence of nifedipine resulted in an increase in the ED50 value of the dose-response curve to B-HT 920 and St587, and this was accompanied by significant reductions of the maximum response, whereas the administration of either staurosporine or nifedipine did not significantly affect the calculated ED50 value of the dose-response curve to cirazoline. In the presence of the calcium channel antagonist but not the PKC inhibitor the maximum response to cirazoline was significantly depressed. As judged from the slope function of the dose-response curves the nature of the inhibition produced by nifedipine compared to staurosporine also appeared to differ. Thus, with nifedipine as the antagonist, the slope function of the dose-response curve for alpha-agonists was significantly reduced. Moreover, in contrast to the actions of staurosporine, nifedipine reduced the maximum response to cirazoline in a dose-independent manner. This study supports the hypothesis that activation of alpha-adrenoceptors that have a substantial dependence on extracellular calcium for vasoconstriction are susceptible not only to the action of calcium channel antagonists but also to the actions of the PKC inhibitor staurosporine, thus suggesting that PKC may modulate directly/indirectly calcium channel activity in vascular smooth muscle.

Adrenergic alpha-Agonists↗

PubMed1990

Effects of beta 1- and beta 2-adrenoceptor stimulation on hemodynamics in the anesthetized rat.

The role of beta 1-adrenoceptors in mediation of vasodilatation is not clear. The microsphere technique was used to compare the effects of mixed beta-, beta 1-, and beta 2-stimulation on blood flow and conductance changes in five groups of pentobarbital-anesthetized rats: I, vehicle; II, mixed beta-stimulation; III, beta 1-stimulation; IV, beta 2-stimulation; and V, mixed beta-blockade. Isoproterenol (32 ng/kg/min) was infused into rats either without (group II) or with ICI 118,551 (beta 2-blocker, 30 micrograms/kg, group III), atenolol (beta 1-blocker, 100 micrograms/kg, group IV), or both blockers (group V), respectively. At the doses selected, ICI 118,551 shifted the dose-vasodepressor response curve of salbutamol (beta 2-agonist) to the right but had no effect on the dose-chronotropic response curve of dobutamine (beta 1-agonist), whereas atenolol shifted the dose-chronotropic response curve of dobutamine to the right and had no effect on the dose-vasodepressor response curve of salbutamol. The results show that isoproterenol increased heart rate (HR) and arterial conductances in the coronary and skeletal muscle beds but had no effects in other beds. Combined with ICI 118,551, isoproterenol caused similar increases in HR and coronary arterial conductance but markedly less increase in skeletal muscle conductance. Atenolol abolished the increase in HR by isoproterenol but did not affect the increases in coronary and muscular arterial conductances. With both blockers, isoproterenol produced no increase in coronary and skeletal muscle conductance. Therefore, both beta 1- and beta 2-adrenoceptors play a role in coronary and skeletal muscle vasodilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

PubMed1990

Effects of nifedipine, BAY K 8644, and pertussis toxin on pressor response to sarafotoxin-b in pithed rats.

The pressor actions of sarafotoxin-b (SRTX-b) were examined in pithed rats in the presence of the calcium channel antagonist nifedipine or the calcium channel activator BAY K 8644 intraarterially (i.a.) and also after pretreatment with pertussis toxin intravenously (i.v.). SRTX-b produced dose-dependent pressor effects in the pithed rat. The diastolic blood pressure (DBP) recorded in animals treated with the vehicle was 41 +/- 1 mm Hg; administration of BAY K 8644 0.1 or 0.3 mg/kg increased DBP pressure to 50 +/- 1 and 52 +/- 1 mm Hg, respectively, whereas nifedipine 0.1 or 0.3 mg/kg decreased DBP to 39 +/- 1 and 33 +/- 1 mm Hg, respectively. The actions of SRTX-b were significantly inhibited by nifedipine, whereas BAY K 8644 potentiated the pressor actions of SRTX-b. We observed that animals pretreated with pertussis toxin 25 or 50 micrograms/kg 3 days before we conducted the experiments had significantly lower DBP as compared with saline-treated animals. Treatment with pertussis toxin caused the DBP dose-response curve to SRTX-b to be displaced to the right. These results indicate that a nifedipine-sensitive (presumably extracellular) calcium pool is partly responsible for the pressor response induced by SRTX-b. They further suggest that in vascular smooth muscle, at least in some vascular beds, SRTX-b activates a pertussin toxin-sensitive G-protein that is coupled to a receptor-operated calcium or nonspecific cation channel.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1990

Adrenalectomy abolishes antagonism of alpha-adrenoceptor-mediated hypotension by a beta-blocker in conscious rats.

1. The effects of a single bolus injection of propranolol, atenolol or ICI 118,551, non-selective beta-, selective beta 1- and selective beta 2-adrenoceptor antagonists, respectively, on mean arterial pressure (MAP) and plasma catecholamine concentrations were examined in seven groups of conscious and unrestrained adrenalectomized rats receiving a continuous infusion of the alpha-adrenoceptor antagonist phentolamine. In all rats adrenaline was undetectable in the plasma four days after adrenalectomy. 2. In the first three groups, phentolamine significantly decreased MAP and increased the plasma concentrations of noradrenaline. The injection of propranolol, atenolol or ICI 118,551 in Groups I, II and III, respectively, caused a small increase in MAP and a small, but not significant, decrease in plasma noradrenaline concentrations. 3. Groups IV, V and VI were given a continuous infusion of adrenaline for 1 h prior to the infusion of phentolamine, followed by a bolus injection of propranolol, atenolol or ICI 118,551, respectively. Group VII was treated similarly to IV, but was also given daily cortisone replacement after adrenalectomy. Adrenaline slightly, but not significantly, decreased MAP while phentolamine significantly decreased MAP and increased plasma noradrenaline concentrations in all groups. A subsequent injection of a beta-blocker caused a significant increase in MAP in each group and a slight decrease in the plasma level of noradrenaline which reached statistical significance in group VII. The pressor effect of propranolol was significantly greater in the cortisone-treated rats (Group VII) than in Group IV. 5. The results suggest that adrenaline and adrenocortical steroids are both involved in the antagonism of alpha-adrenoceptor-induced hypotension by a beta-blocker.

Adrenal Glands↗

PubMed1990

Comparison between the vasoactive actions of endothelin and arginine vasopressin in pithed rats after pretreatment with BAY K 8644, nifedipine or pertussis toxin.

Both human endothelin 1 (ET1) and rat endothelin 3 (ET3) produced dose-dependent pressor effects in the pithed rat. The pressor actions of ET3 and arginine vasopressin (AVP) were compared with one another in pithed rats in the presence of the calcium channel activator BAY K 8644 or the calcium channel antagonist nifedipine i.a. and also after pretreatment with pertussis toxin i.v. The diastolic pressure recorded in animals treated with the vehicle was 41 +/- 1 mm Hg, and administration of BAY K 8644 increased the diastolic pressure to 53 +/- 3 mm Hg, whereas nifedipine caused a decrease in diastolic pressure to 33 +/- 2 mm Hg. AVP, ET1 and ET3 dose-dependently increased diastolic blood pressure, with AVP being the most potent and producing the greatest total increase in pressure. ET1 was more potent than ET3; however, the maximal increases produced by the endothelins were identical. The actions of ET3 but not AVP were potentiated in the presence of BAY K 8644. Furthermore, nifedipine significantly impaired responses induced by endothelin but not those produced by AVP. It was observed that animals treated with pertussis toxin 3 days before the conduction of the experiments had a significantly lower diastolic blood pressure as compared with saline-treated animals. Treatment with pertussis toxin caused the dose-diastolic pressure response curve to ET to be displaced to the right, whereas the dose-diastolic pressure response to AVP was not affected.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1989

Effects of vasodilator drugs on venous tone in conscious rats.

The dose-response effects of vasodilator drugs, nitroglycerin, sodium nitroprusside and hydralazine, on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of body venous tone, were investigated in conscious, unrestrained, intact rats as well as in rats treated with the ganglionic blocker, hexamethonium. The effects of these drugs were compared with those of the vehicle, normal saline, in control rats. In intact rats, i.v. infusion of nitroglycerin did not alter MAP while i.v. infusions of nitroprusside or hydralazine caused dose-dependent decreases in MAP. After ganglionic blockade, all three drugs decreased MAP. In intact rats, nitroglycerin and sodium nitroprusside did not affect MCFP but hydralazine increased MCFP. After treatment with hexamethonium, all three drugs decreased MCFP. The decreases in MCFP caused by nitroglycerin and nitroprusside, but not that by hydralazine, were significantly greater than the corresponding changes in control rats. Thus, in intact rats, the direct venodilator actions of nitroprusside and nitroglycerin were masked by endogenous sympathetic tone. When sympathetic nerve activity was attenuated, both nitroprusside and nitroglycerin have venodilator effects. Hydralazine, on the other hand, had insignificant venodilator effect both in the presence and absence of sympathetic reflexes.

Animals↗

PubMed1989

Benextramine and nifedipine distinguish between sub-classes of alpha 1-adrenoceptors.

The effects of benextramine and nifedipine were examined on the dose-diastolic pressure response to methoxamine in pithed normotensive rats. Benextramine (3, 6 and 12 mg/Kg) displaced the dose-response curve to methoxamine to the right. Maximum response was reduced after the administration of 12 mg/Kg benextramine. Nifedipine (0.1 and 0.3 mg/Kg) also caused the dose-response curve to methoxamine to be displaced to the right with reduction in maximum response. Nifedipine effects were additive with an increase in the EC50 values as well as reduction in the maximum response after pretreatment with benextramine (3 and 6 mg/Kg). However, at the highest dose of benextramine the effects of nifedipine were diminished and no longer apparent. It is concluded that benextramine may have alkylated a nifedipine sensitive site on the alpha 1-adrenoceptors.

Animals↗

PubMed1989

Effects of anipamil on cardiovascular status and regional blood flow in anaesthetized rats.

1. Anipamil, a long-acting analogue of verapamil, was tested at 1, 2.5 and 5 mg kg-1 i.v. for its effects on cardiovascular status and blood flow in different organs and vascular beds in rats anaesthetized with pentobarbitone. 2. Blood flow was determined by microsphere (57Co or 113Sn) injection before, and 1 h after, administration of anipamil at the above doses. 3. Anipamil produced a dose-dependent fall in blood pressure and heart rate. This was associated with a fall in peripheral resistance. At the highest dose there was, in addition, evidence of myocardial depression. 4. Both blood flow and conductance (flow corrected for blood pressure) were notably increased by anipamil in heart, liver and skeletal muscle beds, but were decreased, especially at the high doses, in kidneys, intestine and spleen. 5. The profile of the actions of anipamil on haemodynamic performance and flow was consistent with its proposed calcium antagonist actions. This profile was similar to that of verapamil.

Anesthesia↗

PubMed1989

Propranolol antagonizes hypotension induced by alpha-blockers but not by sodium nitroprusside or methacholine.

A pressor response has been observed with propranolol, a nonselective beta-adrenoceptor antagonist, in animals given a nonselective alpha-adrenoceptor antagonist. This study investigates whether a pressor response to propranolol occurs in conscious unrestrained rats following a hypotensive response induced by phentolamine (nonselective alpha-antagonist), prazosin (selective alpha 1-antagonist) and (or) rauwolscine (selective alpha 2-antagonist), sodium nitroprusside (smooth muscle relaxant), or methacholine (muscarinic agonist). The rats were subjected to a continuous infusion of a hypotensive agent or normal saline followed by i.v. injection of propranolol. The infusion of phentolamine significantly decreased mean arterial pressure (MAP). Subsequent injection of propranolol restored MAP to the control level. Prazosin and rauwolscine each caused a small but not significant decrease in MAP which was reversed by propranolol. Concurrent infusions of prazosin and rauwolscine caused a significant decrease in MAP. Subsequent injection of propranolol caused a large pressor response which increased MAP to 20% above control MAP prior to the administration of drugs. Nitroprusside or methacholine each caused a significant decrease in MAP, but the hypotension was not antagonized by propranolol. The concurrent infusions of a low dose of nitroprusside and prazosin caused a significant decrease in MAP which was reversed by propranolol. The infusion of saline did not alter MAP, and propranolol did not cause a pressor response. It is concluded that propranolol antagonizes the hypotensive effect of an alpha-blocker but not that of sodium nitroprusside or methacholine. Our results suggest the presence of a specific interaction between alpha- and beta-antagonists.

Adrenergic alpha-Antagonists↗

PubMed1988

[Sar1Ile7]angiotensin III, a new selective antagonist of the pressor effect of angiotensin III in conscious rats.

Two analogues of angiotensin III were compared as antagonists of the pressor response to angiotensin II (ANG II) and angiotensin III (ANG III) in conscious, unrestrained rats. Dose-mean arterial pressure (MAP) response curves were obtained for ANG II and ANG III in the absence or presence of [Ile7]ANG III (1.3 x 10(-7) mol/kg) or [Sar1 Ile7]ANG III (1.2 x 10(-7) mol/kg). In the presence of [Ile7]ANG III, the dose-MAP response curves for ANG II and ANG III were significantly displaced to the right. [Ile7]ANG III behaved as a partial agonist on ANG II but not ANG III receptors. In the presence of [Sar1 Ile7]ANG III, the dose-MAP response curve for ANG III but not ANG II was significantly displaced to the right. This suggests that [Sar1 Ile7]ANG III is a selective antagonist of ANG III in the vasculature. [Ile7]ANG III, on the other hand, antagonizes both ANG II and ANG III receptors. Our results support the hypothesis of the existence of a sub-class of angiotensin receptors activated by ANG III in the vascular smooth muscle.

Angiotensin II↗

PubMed1988

Pressor response to beta 1- and beta 2-blockers in conscious rats treated with phentolamine.

The purpose of this study was to examine the conditions whereby beta-blockers cause a pressor response in conscious, unrestrained rats: (1) whether beta-blockers cause a pressor response in rats subjected to, or not subjected to, nonselective alpha-blockade with phentolamine; (2) whether the pressor response to beta-blockers is due to the blockade of vasodilator beta 2-adrenoceptors, and (3) whether it is due to an acute increase in the release of adrenaline (A) and noradrenaline (NA). In the first series of experiments cumulative dose-response curves for propranolol, atenolol and ICI 118,551, nonselective beta-, beta 1- and beta 2-selective antagonists, respectively, were constructed in rats subjected to a continuous intravenous infusion of phentolamine. The administration of each of the beta-antagonists caused a significant dose-dependent increase in mean arterial pressure (MAP). The ED50 values for the increase in MAP were found to be 3.6 +/- 0.8, 10 +/- 2.6 and 4.6 +/- 0.8 micrograms/kg for propranolol, atenolol and ICI 118,551, respectively. In the second series of experiments, a single bolus injection of a selective or nonselective beta-antagonist or saline vehicle was given to rats subjected to a continuous intravenous infusion of phentolamine. Plasma levels of A and NA were determined in the control condition, during the infusion of phentolamine and again after the injection of a beta-antagonist. The infusion of phentolamine significantly decreased MAP and increased plasma levels of A and NA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed1987

Are angiotensin receptors in vascular smooth muscles a homogeneous population?

The effects of angiotensin II (AII) and angiotensin III (AIII) on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of total body venous tone, in the presence and absence of [Sar1,Ile8]AII in conscious rats were examined. The infusion of AII caused dose-dependent increases in MAP and MCFP. The dose-response curves of MAP and MCFP for AII were displaced to the right in the presence of various doses of [Sar1,Ile8]AII. The pA2 values obtained for AII in the presence of the antagonist were 9.2 and 8.4 for the arterioles and veins respectively. The infusion of AIII also caused dose-dependent increases in MAP and MCFP. In the presence of the antagonist the AIII dose-response curves for MAP and MCFP were not displaced to right. The same maximum MAP was obtained for both AII and AIII but the maximum MCFP obtained following the infusion of AIII was smaller than that for AII. It is concluded that AII may act on different sub-classes of angiotensin receptors in arterioles and veins. AIII caused vasoconstriction in arterioles by acting on a sub-class of angiotensin receptors different from the ones activated by AII. AIII may act as a partial agonist on the same types of receptors as AIII in the venous bed.

Angiotensin II↗

PubMed1987

Investigation of the central and peripheral actions of clonidine and methoxamine using a new in vivo rat preparation.

A cross-circulation technique was developed in rats to distinguish central from peripheral cardiovascular actions of drugs. The right common carotid arteries were ligated, and the left common carotid arteries and left and right external jugular veins of two pentobarbital-anesthetized rats were connected with PE tubing so that peripheral blood from one rat, A, supplied the head of another rat, B, and then returned to the body of A, and vice versa, for peripheral blood from rat B. Each rat was artificially ventilated with O2, the chest was opened, and both subclavian arteries were ligated. The distribution of blood flow was verified by the microsphere technique. Prior to ligation of the subclavian arteries, blood flow from rat A supplied its own brain and both brain hemispheres but not the brain stem of rat B. Following subclavian artery ligation, blood flow from rat A did not supply A's brain, but supplied both hemispheres and the brain stem of rat B. The head of each rat was, therefore, rendered dependent on the carotid arterial blood supply from another rat. The i.v. injection of clonidine (25 micrograms/kg) into rat A significantly increased mean arterial pressure and slightly, but not significantly, decreased heart rate in rat A, whereas it significantly decreased mean arterial pressure and slightly, but not significantly, decreased heart rate in rat B. Conversely, i.v. injection of methoxamine (25 micrograms/kg) in rat A significantly increased mean arterial pressure and decreased heart rate in rat A, and significantly increased mean arterial pressure and slightly, but not significantly, increased heart rate in rat B. Therefore, this rat cross-circulation preparation can be used to separate the central and peripheral cardiovascular actions of drugs.

Animals↗

PubMed1987

Comparative effects of rauwolscine, prazosin, and phentolamine on blood pressure and cardiac output in anesthetized rats.

The endogenous role of the alpha-adrenergic system in the maintenance of mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO) and its distribution, and plasma norepinephrine and epinephrine release was investigated by the administration of selective alpha-adrenoceptor antagonists to halothane-anesthetized rats. The blockade of alpha 1-, alpha 2-, and both alpha 1- and alpha 2-receptors was accomplished by i.v. infusions of prazosin, rauwolscine, and phentolamine, respectively. The microsphere technique was used for the determination of CO and its distribution. Since the infusions of the three antagonists caused similar decreases of MAP and heart rate, the results suggest that postjunctional alpha 1- and alpha 2-receptors are both important in the control of MAP. During the infusion of prazosin, TPR was decreased but CO was not changed. In contrast, CO was decreased but TPR was not changed during the infusions of rauwolscine and phentolamine. Thus, CO was reduced after the blockade of alpha 2- but not alpha 1-receptors. All three antagonists caused an increase in percent distribution of CO to the lungs and muscle, suggesting that the sympathetic nervous system plays the greatest vasoconstrictor influence in the lungs and muscle via stimulations of both subtypes of alpha-adrenoceptors. The administration of either prazosin or rauwolscine caused little change in plasma catecholamine levels. In contrast, phentolamine caused large increases in both epinephrine and norepinephrine levels. Therefore catecholamine release was only increased after concurrent blockade of both alpha 1- and alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗

PubMed1986

An improved perfusion apparatus for small animal hearts.

A perfusion apparatus for mechanical and electrophysiological studies in small animal (e.g., rat, guinea pig) hearts is described. The apparatus consists of a number of individual perfusion chambers connected to the aortic perfusion cannula of a Langendorff perfused heart. The aortic root perfusion pressure is controlled by the oxygenating gas (usually 5% CO2 in O2) at a range of 0-200 mmHg. Different solutions can be placed in different individual chambers. Pressure in the left ventricle is monitored by means of a special compliant, but nonelastic, balloon while special atraumatic electrodes allow high-voltage, noise-free ECG recordings to be made from all parts of the epicardium. The apparatus keeps hearts beating for hours while the multichamber allows multiple drug applications to be made rapidly. Thus, the apparatus can be used for all types of pharmacodynamic analysis.

Animals↗

PubMed1986

The effects of noradrenaline, B-HT 920, methoxamine, angiotensin II and vasopressin on mean circulatory filling pressure in conscious rats.

The effects of vasoactive substances on mean circulatory filling pressure (MCFP), an index of total body venous tone, were determined in conscious rats. Cumulative doses of saline (0.9% w/v NaCl solution), methoxamine (alpha 1-adrenoceptor agonist), B-HT920 (alpha 2-adrenoceptor agonist) noradrenaline and vasopressin, and individual doses of angiotensin II (AII), were infused into the rats. Mean arterial pressure (MAP), MCFP and heart rate (HR) were determined before and during the plateau responses to infusions of the vasoactive substances. The infusions of all the agonists caused a dose-dependent increase in MAP and a decrease in HR. The infusion of saline affected neither MAP nor HR. The infusions of saline and methoxamine did not affect MCFP while the infusions of B-HT 920, noradrenaline and AII increased MCFP. MCFP was slightly increased during the infusion of high doses of vasopressin. It was concluded that receptors for the alpha 2-adrenoceptor agonist and AII are involved in the control of venous tone. Receptors for the alpha 1-adrenoceptor agonist and vasopressin are not important for the control of venous tone.

Adrenergic alpha-Agonists↗