Biomedical subjects

C C Pang

Publications and source records attributed to C C Pang.

At least 91 records · Page 5Linked to original sources

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

Effects of calcium antagonists on mean circulatory filling pressure in the conscious rat.

The effects of three calcium antagonists (verapamil, nifedipine, and flunarizine) on mean arterial pressure (MAP), heart rate (HR), and mean circulatory filling pressure (MCFP), an index of total body venous tone, were investigated in the conscious, unrestrained rat. Infusions of all three drugs caused a dose-dependent decrease in MAP and an increase in MCFP, compared with the corresponding values in control rats. HR was decreased by verapamil and flunarizine and slightly increased by nifedipine. Further experiments investigated whether the increase in MCFP by verapamil was indirectly caused by reflex activation of the sympathetic nervous system. Rats were pretreated with a continuous infusion of hexamethonium prior to the infusion of verapamil. After treatment with hexamethonium, verapamil did not increase the MCFP. In fact, the highest dose of verapamil significantly decreased MCFP. The results suggest that calcium antagonists have greater dilator effects in arterioles compared to veins. It appears that any direct venodilator effects of verapamil in conscious rats are masked due to reflex activation of the autonomic nervous system.

Animals↗

PubMed1988

Differential cardiovascular effects of central clonidine and B-HT 920 in conscious rats.

The effect of intracerebroventricular (i.c.v.) injection of the alpha 2-adrenoceptor agonists clonidine and B-HT 920 on mean arterial pressure (MAP), heart rate (HR), and plasma concentrations of noradrenaline and adrenaline was examined in conscious unrestrained rats. The injection of 1.0 microgram clonidine significantly decreased MAP and slightly decreased HR. Plasma noradrenaline and adrenaline levels were slightly but not significantly decreased after the injection of 1 microgram clonidine. In contrast, the injection of 0.1-10.0 micrograms B-HT 920 increased MAP and decreased HR. Plasma noradrenaline and adrenaline levels were slightly increased after the injection of the 1- and 10-micrograms doses. The i.c.v. injection of the alpha 2-antagonist rauwolscine slightly but not significantly increased MAP and plasma noradrenaline and adrenaline levels. The responses to i.c.v. injection of clonidine and B-HT 920 were not changed by prior administration of rauwolscine. Neither the pressor response to B-HT 920 nor the depressor response to clonidine was abolished by rauwolscine, suggesting that neither response was mediated by alpha 2-adrenoceptors.

Animals↗

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

Cardiovascular effects of injections of vasopressin into the nucleus tractus solitarius in conscious rats.

The effects of injections of arginine vasopressin (AVP) into the nucleus tractus solitarius (NTS) on mean arterial pressure (MAP), heart rate (HR) and plasma concentrations of noradrenaline and adrenaline were investigated in conscious, unrestrained rats. Injection of 2 ng AVP into the NTS significantly increased MAP but not plasma catecholamine concentrations, while injection of 10 ng AVP significantly increased MAP and plasma noradrenaline and adrenaline levels. Neither dose of AVP produced any change in HR. The vehicle did not affect MAP, HR or plasma catecholamine levels. Injection of a specific pressor antagonist of AVP, d(CH2)5Tyr-(Me)AVP (10 ng), did not change MAP, HR or plasma noradrenaline or adrenaline levels. These results suggest that the NTS is a central site of the pressor action of AVP. However, since the injection of the AVP antagonist did not reduce MAP or plasma noradrenaline or adrenaline levels, it suggests that AVP does not act tonically at the NTS to influence sympathoadrenal outflow.

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

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↗

PubMed1986

Vascular role of vasopressin in the presence and absence of influence from angiotensin II or alpha-adrenergic system.

The effects of a vasopressin (AVP) pressor antagonist, d(CH2)5Tyr(Me)AVP, on mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO), and the distribution of CO were investigated by the microsphere technique in three groups of pentobarbital anesthetized rats: intact (I), saralasin pretreated (II), and phentolamine pretreated (III). Saralasin and phentolamine were infused intravenously to inactivate the renin-angiotensin and alpha-adrenergic systems, respectively. The AVP antagonist decreased MAP and TPR in all groups and it caused a greater depressor effect in groups II and III than in group I. In group I, AVP antagonist increased blood flow (BF) to the stomach and skin. In group II, AVP antagonist increased BF to the muscle and skin. In group III, AVP antagonist markedly increased BF to the muscle. Therefore, the degree of vasoconstrictor influence exerted by AVP in different vascular beds varies depending on endogenous vasomotor tone from the renin-angiotensin and (or) sympathetic nervous systems.

Animals↗

PubMed1985

Differential intraarterial pressure recordings from different arteries in the rat.

Intraarterial pressures were recorded from five different sites in pentobarbital anesthetized rats. Simultaneous recordings were made from the brachial artery, carotid artery, femoral artery, tail artery, and a small end-branch of the superior mesenteric artery under basal conditions and under vasoconstrictor and vasodilator influences to find out whether similar mean arterial pressures (MAP) can be recorded from the various sites. It was found that MAP of proximal arteries (brachial and carotid) is higher than the MAP recorded from more distal arteries (mesenteric, tail, and femoral). A pressure difference of 5-6 mm Hg was found to exist from the level of the carotid artery to that of the femoral artery during all experimental conditions. Our results indicate that the same artery should always be used to compare MAP between different rats. Moreover, calculations of arterial resistance (MAP/BF) of most vascular beds in the rat, using MAP values obtained from the tail or the femoral artery, as are commonly done in physiologic or pharmacologic studies, can result in slightly lower resistance values than the true resistance. To obtain true arterial resistance of any vascular bed, one has to use MAP recorded at the particular vascular bed for the calculation of resistance.

Animals↗

PubMed1985

Chronic treatment of rats with D-600 causes a compensatory decrease in the calcium requirement for contractility of vascular smooth and cardiac muscles.

We studied the effects of chronic hypotensive treatment of normotensive Wistar rats (NWR) with methoxyverapamil (D-600) and hydralazine on in vitro contractile response of aortic strips, portal vein strips, and Langendorff-perfused hearts in normal (2.5 mM) and low (0.2 mM) calcium (Ca). Portal vein strips from rats treated with D-600, compared with the same strips from control and hydralazine-treated rats, developed greater spontaneous contractile activity in normal Ca and retained greater responses to norepinephrine (NE) and 80 mM K in low Ca. Aortic strips from all three groups of rats retained similar responses to NE and K in low Ca. Hearts from D-600-treated rats produced less intraventricular pressure (IVP) to isoproterenol (ISO) than hearts from control and hydralazine-treated rats in normal Ca but greater IVP to ISO than hearts from the other two groups of rats in low Ca. Thus, chronic treatment of NWR with D-600 but not with hydralazine resulted in the reduction of Ca requirement for contractile activities of the portal vein and the myocardium.

Animals↗

PubMed1985

Central vasopressin in the modulation of catecholamine release in conscious rats.

Neurons containing arginine vasopressin (AVP) have been shown to project from the paraventricular nucleus of the hypothalamus to the nucleus tractus solitarius (NTS) in the medulla. We investigated whether AVP acts in brain stem regions to influence sympathoadrenal outflow. Cannulae were implanted into the fourth ventricle of rats 7 days prior to the experiment. The effects of intracerebroventricular (icv) injections of AVP, the vehicle, and AVP antagonist, d(CH2)5Tyr(Me)AVP, on mean arterial pressure (MAP) and plasma noradrenaline (NA) and adrenaline (A) levels were determined in conscious unrestrained rats. Injections of AVP (icv, 23 and 73 ng/kg) but not the vehicle increased MAP and plasma NA and A levels. In contrast, iv injection of AVP increased MAP but decreased plasma concentrations of A and NA. The pressor response to icv injection of AVP was abolished by prior icv injection of AVP antagonist. Injection of AVP antagonist (icv, 0.5 and 1.5 microgram/kg) had no effect on MAP or plasma NA or A levels. These results show that centrally injected AVP activates sympathoadrenal outflow, possibly via an inhibition of baroreceptor reflexes. Since centrally administered AVP antagonist did not influence MAP or plasma NA or A levels, it appears that endogenously released AVP does not have a tonic influence on central cardiovascular reflex system in conscious, unrestrained rats.

Animals↗

PubMed1983

Vasopressin and angiotensin in the control of arterial pressure and regional blood flow in anaesthetized, surgically stressed rats.

The effects of vasopressin and angiotensin II in the control of regional blood flow (BF) in halothane-anaesthetized rats were investigated by the administration of specific antagonists of vasopressin and angiotensin II, namely, [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine] arginine-vasopressin [d(CH2)5 Tyr(Me) AVP] and saralasin, respectively. Cardiac output and the distribution of BF was examined by the reference sample microsphere technique. The injection of the vasopressin antagonist into the left ventricle of rats caused reductions of mean arterial pressure (MAP) and total peripheral resistance (TPR), an increase of BF to the stomach and skin and a decrease of BF to the intestine. Intravenous infusion of saralasin caused reductions of MAP and TPR and an increase of BF to the kidneys and skin. The results show that both the vasopressin and the renin-angiotensin systems participate in the control of arterial pressure and peripheral vascular resistance in anaesthetized, surgically stressed rats.

Anesthesia↗

PubMed1983

Effect of vasopressin antagonist and saralasin on regional blood flow following hemorrhage.

The effects of hemorrhagic hypotension on mean arterial pressure (MAP), cardiac output (CO), and its distribution were investigated in halothane-anesthetized rats using the radioactive microsphere technique. Hemorrhage (12 ml/kg) decreased MAP and CO, increased total peripheral resistance (TPR), and decreased blood flow (BF) to the heart, stomach, intestine, kidneys, skin, cecum, and colon. The effects of antagonists of vasopressin and the renin-angiotensin system on peripheral circulation following hypotensive hemorrhage were also examined using d(CH2)5Tyr(Me)AVP and saralasin, respectively. Injection of the vasopressin antagonist caused a reduction of MAP by reducing TPR and caused an increase of percent distribution of CO to the stomach, skin, cecum, and colon. Intravenous infusion of saralasin caused significant reductions of MAP by reducing TPR. Saralasin caused an increase of percent distribution of CO to the kidneys. The results show that both vasopressin and the renin-angiotensin systems participate in the control of MAP and peripheral vascular resistance following hypotensive hemorrhage in anesthetized rats.

Animals↗

PubMed1982

Effect of pentobarbital anesthesia and surgery on the control of arterial pressure and mesenteric resistance in cats: role of vasopressin and angiotensin.

We compared the effects of pentobarbital-induced anesthesia and major surgery (laparotomy) on the mesenteric resistance vessels and arterial pressure of cats. Intravenous infusion of sodium pentobarbital (30 mg/kg over 30--60 min) into conscious and unrestrained cats caused only a small increase in superior mesenteric arterial conductance and a small fall in femoral arterial pressure. In contrast to the effects of pentobarbital, major surgery caused marked mesenteric vasoconstrictor and pressor responses. Under these conditions, acute hypophysectomy and infusion of [Sar1, Ala8]angiotension II (saralasin) caused mesenteric conductance and arterial pressure to return towards presurgery control values. The results suggest that the high arterial pressure and constricted state of the mesenteric bed seen in acute experiments appears to be related to surgical stress rather than pentobarbital-induced anesthesia and that both the vasopressin system and the renin-angiotensin system appear to play important roles in the control of arterial pressure and the mesenteric resistance vessels under these conditions.

Anesthesia↗

PubMed1981

Prolonged inhibition of pressor response to vasopressin by a potent specific antagonist, [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]arginine-vasopressin.

The specificity, the potency, and the duration of action of [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]arginine-vasopressin[d(CH2)5Tyr(Me)AVP] to antagonize pressor responses to arginine vasopressin (AVP) was examined in pentobarbital-anaesthetized rats. Injection of the compound (4 micrograms.kg-1 i.v.) prevented pressor responses to i.v. infusions of supramaximal doses of AVP, but not to i.v. infusions of another peptide, angiotensin II (Ag II). The antagonism of AVP persisted for at least 3 h. Since i.v. injection of the compound in the absence of exogenous administration of AVP did not cause any change in the arterial pressure of rats, it appears that the compound is devoid of agonistic pressor activity. The results show that d(CH2)5Tyr(Me)AVP is a potent and a specific antagonist of pressor responses to AVP.

Animals↗

PubMed1981

Differential effects of D 600 on contractile response of aorta and portal vein from spontaneously hypertensive rats.

To examine if Ca handling by vascular smooth muscles is altered in hypertension, the in vitro effect of D 600 was determined on noradrenaline-induced contractions of aortic and portal vein strips from spontaneously hypertensive rats (SHR) and Wistar Kyoto normotensive rats (WKY). In low (0.2 and 0.4 mM) Ca solutions, D 600 reduced the response to noradrenaline to a greater extent in aortic strips from SHR than in strips from WKY. In contrast, D 600 had less effect on the response to noradrenaline in portal vein strips from SHR than in strips from WKY in both normal and low Ca. Thus, portal veins from SHR are less dependent on external Ca compared to portal veins from WKY whereas aortae from SHR are more dependent on external Ca compared to aortae from WKY.

Animals↗