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Biomedical subjects

C C Pang

Publications and source records attributed to C C Pang.

At least 73 records · Page 4Linked to original sources
PubMed1992

The sympathetic nervous system facilitates endothelin-1 effects on venous tone.

The effects of endothelin-1 (ET-1) or normal saline (0.9% NaCl) on mean arterial pressure (MAP), heart rate (HR) and mean circulatory filling pressure (MCFP), an index of body venous tone, were studied in 10 groups (n = 6 each) of conscious, unrestrained rats continuously i.v. infused with vehicle, verapamil, both hexamethonium and verapamil, phentolamine or, both phentolamine and verapamil. Infusion (i.v.) of normal saline into the five control groups did not significantly alter MAP, HR or MCFP. Cumulative i.v. bolus of ET-1 (0.8, 1.6, 3.2, 6.4, 12.8 and 19.4 x 10(-10) mol/kg) reduced HR in all five treatment groups and dose-dependently increased MAP in the presence of either vehicle or phentolamine, but did not affect MAP in the groups treated with verapamil. The ability of ET-1 to reduce HR in verapamil-treated rats, despite the absence of a pressor response, suggests that ET-1 is negatively chronotropic. ET-1 alone slightly increased MCFP and it did not alter MCFP in the presence of phentolamine. In the presence of verapamil, ET-1 markedly raised MCFP, and this was abolished by concurrent treatment with either hexamethonium or phentolamine. Therefore, ET-1 markedly elevates venous tone in the presence of verapamil via reflex-mediated increase in sympathetic nerve activity and the activation of alpha adrenoceptors.

Animals↗
PubMed1991

Effects of neuropeptide Y on mean circulatory filling pressure in intact and ganglionic-blocked conscious rats.

The dose-response effects of neuropeptide Y (NPY) and the vehicle, 0.9% NaCl, on mean arterial pressure (MAP), heart rate (HR) and mean circulatory filling pressure (MCFP), an index of body venous tone, were examined in conscious, intact and hexamethonium-treated rats. Saline infusions in intact and hexamethonium-treated rats did not significantly affect MAP, HR and MCFP. The i.v. infusion of NPY in intact rats dose dependently increased MAP, decreased HR, but did not alter MCFP. In the presence of hexamethonium, the pressor effect of NPY was enhanced, the lack of MCFP effect remained and the bradycardic effect was markedly attenuated. Our results suggest that NPY has moderate effects on MAP, but negligible effects on body venous tone.

Animals↗
PubMed1991

Pressor effects of L and D enantiomers of NG-nitro-arginine in conscious rats are antagonized by L- but not D-arginine.

The effects of NG-nitro-L-arginine (L-NNA) and NG-nitro-D-arginine (D-NNA) on mean arterial pressure (MAP) were studied in conscious, unrestrained rats. I.v. bolus of either L-NNA (1-64 mg/kg) or D-NNA (2-64 mg/kg) dose dependently increased MAP to similar maximum values of 55 +/- 7 and 52 +/- 4 mm Hg and with ED50 values of 4.0 +/- 0.9 and 8.9 +/- 1.2 mg/kg (P less than 0.05), respectively. The time course of the MAP response to a single dose (32 mg/kg i.v. bolus) of L-NNA and D-NNA were also obtained. The pressor effects of L-NNA and D-NNA each lasted greater than 2 h with the rise phase t 1/2 of 5 and 27 min (P less than 0.05), respectively. I.v. infusions (10 mg/kg per min) of L-arginine (L-Arg) and D-arginine (D-Arg) did not alter the pressor response to noradrenaline nor angiotensin II. L-Arg but not D-Arg attenuated the pressor responses to both L-NNA and D-NNA. Therefore, both L-NNA and D-NNA are efficacious and long-lasting pressor agents; the pressor effects of both can be antagonized by L-Arg but not D-Arg. Our results suggest that the pressor effects of both L-NNA and D-NNA involve the L-Arg/nitric oxide pathway.

Animals↗
PubMed1991

Effects of inhalation and intravenous anesthetic agents on pressor response to NG-nitro-L-arginine.

The effects of anaesthetic agents on pressor effect of NG-nitro-L-arginine (L-NNA), a potent inhibitor of nitric oxide (NO) synthesis, were examined in rats. I.v. bolus of L-NNA (1-32 mg/kg) in conscious rats dose dependently increased mean arterial pressure (MAP) to a maximum value of 53 +/- 2 mmHg at 16 mg/kg with ED50 value of 4.7 +/- 0.9 mg/kg. The effects of a single i.v. bolus dose (32 mg/kg) of L-NNA were examined in conscious rats and rats anaesthetised with pentobarbital, chloralose, ketamine, althesin (mixture of alphaxalone and alphadolone), urethane, enflurane or halothane. In conscious rats, peak MAP (51 +/- 3 mmHg) was reached 10 min after i.v. injection and the effect lasted more than two hours. The magnitudes of peak MAP differed under the influence of anaesthetic agents with the following rank order: althesin greater than conscious = pentobarbital = chloralose = ketamine = urethane greater than enflurane much greater than halothane (in which there was negligible change in MAP). The onsets were delayed in rats anaesthetised with pentobarbital, althesin, chloralose and enflurane but not altered with ketamine and urethane compared to that in conscious rats. Therefore, L-NNA caused intense and prolonged pressor response in conscious rats and rats anaesthetised with the i.v. anaesthetic agents pentobarbital, chloralose, ketamine, althesin and urethane. MAP effect of L-NNA was markedly attenuated by the inhalation anaesthetics halothane and enflurane.

Alfaxalone Alfadolone Mixture↗
PubMed1991

Possible dependence of pressor and heart rate effects of NG-nitro-L-arginine on autonomic nerve activity.

1. The effects of NG-nitro-L-arginine (L-NNA) on mean arterial pressure (MAP) and heart rate (HR) were investigated in conscious rats. 2. Intravenous bolus cumulative doses of L-NNA (1-32 mg kg-1) dose-dependently increased MAP. Both mecamylamine and phentolamine increased MAP responses to L-NNA, angiotensin II and methoxamine. Propranolol, reserpine, atropine and captopril did not affect MAP response to L-NNA. 3. A significant negative correlation of HR and MAP responses to L-NNA was obtained in control rats but not in rats pretreated with reserpine or mecamylamine. Significant negative correlations also occurred in the presence of atropine, propranolol, phentolamine or captopril. 4. A single i.v. bolus dose of L-NNA (32 mg kg-1) raised MAP to a peak value of 53 +/- 3 mmHg and the effect lasted more than 2 h; the rise and recovery of MAP were accompanied by significant decrease and increase in HR, respectively. While both phentolamine and mecamylamine increased peak MAP response to L-NNA, mecamylamine abolished the biphasic HR response and phentolamine potentiated the bradycardiac component of HR. 5. Blockade of the autonomic nervous and renin-angiotensin systems did not attenuate the pressor effects of L-NNA. However, the biphasic HR response to L-NNA is mediated via modulation of autonomic nerve activities.

Animals↗
PubMed1990

Differential venous effects of isoprenaline in conscious rats.

The role beta-adrenoceptors in the control of venous tone is not clear. This study examines the dose-response effects of isoprenaline, a non-selective beta-adrenoceptor agonist, on mean circulatory filling pressure (MCFP), an index of body venous tone, in conscious and unrestrained rats. Dose-response curves of isoprenaline were constructed in three groups of rats, namely, I, intact; III, pretreated with the ganglionic blocker hexamethonium; and V, pretreated with noradrenaline. Three additional groups, Groups II, IV and VI, served as time controls and were treated similar to I, III and V, respectively, except that they were given normal saline in place of isoprenaline. The infusion of isoprenaline in intact rats dose dependently decreased mean arterial pressure (MAP) and increased heart rate (HR) and MCFP while in the ganglionic-blocked rat, it caused similar effects on MAP and HR but had no significant effects on MCFP. In rats given noradrenaline, isoprenaline again decreased MAP and increased HR and, in contrast to the other two groups, it decreased MCFP. The results show that isoprenaline has variable venous effects depending on existing venous tone. It causes reflex-mediated venoconstriction under normal conditions due to its hypotensive effects and direct venodilatation when venous tone is elevated by the infusion of noradrenaline.

Animals↗
PubMed1990

Effects of alpha 1- and alpha 2-adrenoceptor antagonists on venous tone in conscious rats.

The dose-response effects of hexamethonium, prazosin and rauwolscine - a ganglionic blocker, alpha 1- and alpha 2-adrenoceptor antagonists, respectively - on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of body venous tone, were examined in conscious and unrestrained rats. Prazosin and rauwolscine were also administered to rats after venous tone was elevated by drug-induced hypotension via the infusion of the vasodilator drug hydralazine. The effects of these drugs were compared with those of the vehicle, acidified glucose solution, administered to control rats. In intact rats, i.v. infusions of prazosin and rauwolscine dose dependently decreased MAP; the highest dose of rauwolscine, but not prazosin slightly reduced MCFP. The i.v. infusion of hexamethonium reduced MAP and caused a marked dose-dependent decrease in MCFP. After venous tone was raised by hydralazine, both prazosin and rauwolscine dose dependently decreased MCFP. The decrease in MCFP caused by rauwolscine was significantly greater than that caused by prazosin. Our results show that in the basal condition, the capacitance vessels are somewhat resistant to the effects of alpha-adrenoceptor antagonists in contrast to the effects of ganglionic blockers. After venous tone was raised by reflex mechanisms, both alpha-adrenoceptor antagonists were effective in lowering venous tone, however, the effect of alpha 2-adrenoceptor antagonist is significantly greater than that of alpha 1-adrenoceptor antagonist.

Adrenergic alpha-Antagonists↗
PubMed1990

Reversal of alpha-adrenoceptor blockade by propranolol in isolated rat pulmonary artery.

Pulmonary artery rings were prepared from rats (group I to VI, n = 5-7 per group) in order to investigate if a beta-adrenoceptor antagonist interferes with the effect of alpha-adrenoceptor blockade. In I, four cumulative noradrenaline (NA) dose-response curves (10(-9) to 10(-3) M) were constructed. In II, NA curves were constructed first, without blockers, then in the presence of phentolamine (10(-6) M), then propranolol (10(-8) M), then phentolamine plus propranolol (10(-8) M). III, IV and V were treated similar to II, except that atenolol (10(-8) M), ICI 118,551 (10(-8) M) and propranolol (10(-6) M), respectively, were added instead of propranolol (10(-8) M). In VI, NA (10(-6) M) was added followed by phentolamine and then propranolol (10(-9) to 10(-6) M). Phentolamine shifted the NA curve to the right with an increase in the EC50 value. Propranolol but not atenolol or ICI 118,551, reduced the elevated EC50 values caused by phentolamine. In group VI, the increase in force by NA was reduced by phentolamine; the effect of phentolamine was completely abolished by propranolol. Thus, propranolol interferes with the effect of phentolamine in the rat pulmonary artery.

Adrenergic alpha-Antagonists↗
PubMed1990

Pressor effect of NG-nitro-L-arginine in pentobarbital-anesthetized rats.

The pressor effect of NG-nitro-L-arginine (L-NNA), a potent inhibitor of nitric oxide (NO) synthesis, was studied in pentobarbital anesthetized rats. Iv injections of L-NNA from 0.25 to 8 mg/kg caused bradycardia and a dose-dependent increase in mean arterial pressure (MAP) with a maximal response of 43 +/- 5 mmHg and ED50 value of 1.3 +/- 0.2 mg/kg. The time course of the response to the injection of a single dose of L-NNA was also determined. Peak response was reached 60 min after the injection of a single dose (4 mg/kg, iv) and the effect lasted greater than 5 h. The rising phase of the pressor response was accompanied by slight bradycardia while the recovery phase was associated with significant tachycardia. Iv injections of L-arginine (12.5-200 mg/kg) caused transient dose-dependent reductions in MAP. The pressor effect of L-NNA (4 mg/kg, iv bolus) was dose-dependently attenuated by L-arginine. The results show that L-NNA is an efficacious and long-acting pressor agent and are consistent with the hypothesis that endogenous NO plays an important role in the regulation of blood pressure.

Anesthesia↗
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 endothelin on arterial pressure and venous tone in intact and hexamethonium-treated conscious rats.

The dose-response effects of the potent vasoconstrictor peptide endothelin on mean arterial pressure (MAP), heart rate (HR), and mean circulatory filling pressure (MCFP), an index of body venous tone, were investigated in conscious and unrestrained, intact rats as well as in rats continuously infused with the ganglionic blocker hexamethonium. The dose of hexamethonium selected was that which reduced the reflex tachycardia induced by i.v. injections of acetylcholine by 50%. In intact rats and rats pretreated with hexamethonium, i.v. injections of endothelin caused dose-dependent increases in MAP and decreases in HR. Low doses of endothelin did not affect MCFP while the highest dose in the intact rat, and the two highest doses in hexamethonium-treated rats, caused small but significant increases in MCFP. Our results suggest that endothelin has small effects on body venous tone in contrast to its effectiveness in raising arterial pressure.

Animals↗
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

Effects of verapamil, nifedipine and flunarizine on haemodynamics and regional blood flows in pentobarbitone-anaesthetized rats.

Representative calcium antagonists from proposed class I (nifedipine), class II (verapamil) and class III (flunarizine) have been examined for effects on blood pressure, heart rate, ventricular pressures, ECG, cardiac output and regional blood flow in pentobarbitone-anaesthetized rats. Flow was measured by the microsphere technique. Low and high infusion rates of each drug were chosen to decrease mean arterial pressure by 25 and 40 mmHg, respectively. At equi-depressor infusion rates, all drugs equally decreased total peripheral resistance and slightly increased cardiac output and stroke volume. Heart rate was decreased by verapamil and flunarizine, but increased by nifedipine. Verapamil markedly decreased dP/dtmax of ventricular pressure and prolonged the PR-interval. Flunarizine was similar. Nifedipine decreased dP/dtmax and had no effect on the PR-interval of the ECG. Similar effects on regional blood flow were seen with the three drugs; flow to lungs, heart, liver, skeletal muscle and stomach increased. Correction for blood pressure changes, i.e. conductance, showed that vasodilatation occurred in all regions, with all drugs, except for the skin. Therefore, representatives from three sub-classes of calcium antagonists had similar effects on blood flow but different effects on the heart.

Anesthesia↗
PubMed1990

Hemodynamic changes that accompany the pressor response to propranolol in urethane anesthetized rats subjected to alpha-blockade.

It has been shown that a paradoxical pressor response to a beta-blocker occurs in rats given an alpha-blocker. The dual-isotope microsphere technique was used to investigate the hemodynamic changes that accompany the pressor response to propranolol in phentolamine-treated, urethane-anesthetized rats. Rats were divided into four groups (n = 8 per group): group I received 10 min of saline infusion; group II received intravenous infusion of phentolamine (300 micrograms/kg/min) for 10 min; group III received intravenous injection of propranolol (100 micrograms/kg) after 20 min of phentolamine infusion, and group IV received intravenous injection of saline after 20 min of phentolamine infusion. In groups I and IV, saline did not cause any significant hemodynamic changes. In group II, phentolamine decreased the mean arterial pressure (MAP) and total peripheral resistance (TPR) by 34 +/- 3 mm Hg and 0.28 +/- 0.07 mm Hg/min/ml, respectively. Arterial conductances in the skeletal muscle and skin were increased to 157 and 165% of control values, respectively. Cardiac output and conductances in other tissues and organs were not significantly affected. In rats given phentolamine (group III), propranolol raised MAP (+40 +/- 2 mm Hg) by increasing TPR (+0.41 +/- 0.03 mm Hg/min/ml). Vascular conductances in the skeletal muscle, skin and kidneys were decreased to 38, 57 and 69% of control values, respectively. Conductances in other tissues and organs were not significantly affected. Our results show that propranolol raised MAP by increasing flow resistance, primarily via the reversal of the vasodilator effects of phentolamine in the muscle and skin.

Adrenergic alpha-Antagonists↗
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

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↗