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Biomedical subjects

R C Webb

Publications and source records attributed to R C Webb.

At least 181 records · Page 10Linked to original sources
PubMed1981

Influence of sex difference and oral contraceptives on forearm reactive hyperemia.

Experiments were performed on normal male and female subjects to compare blood flow responses following release of an arterial occlusion (reactive hyperemia). Additionally, the effects of oral contraceptive therapy on the reactive hyperemia reaction were studied in female subjects. Forearm blood flow was measured with a strain-gauge plethysmograph, heart rate with an electrocardiograph, and mean arterial pressure was measured by auscultation. Blood flow was determined before and after circulatory arrest of 1, 3, and 5 min. Blood serum levels of 17 beta-estradiol, progesterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) were measured by radioimmunoassay. The mean resting forearm blood flow was similar in males and females (approximately 4 ml/100 ml/min). There were no significant changes in systemic mean arterial pressure or heart rate during the experiments. Following 1 min of arterial occlusion, the peak blood flow responses were similar in males and females. The peak blood flow responses following release of arterial occlusion were lower in males than in untreated females at occlusion intervals of 3 and 5 min. Females receiving oral contraceptives showed reduced peak blood flow responses after circulatory arrest of either 3 or 5 min as compared to untreated females. There were no significant differences in the recovery times of the hyperemic responses between males and females following any of the periods of occlusion. The peak blood flow responses following 3 min of arterial occlusion were significantly correlated with the blood serum levels of 17 beta-estradiol, LH and FSH, but not with the blood serum levels of progesterone. These results suggest that: (1) sex difference has a marked effect on the blood flow response following arterial occlusion, and (2) hormonal changes influence vascular responsiveness in the female.

Blood Pressure↗
PubMed1981

Relaxation of vascular smooth muscle by isoproterenol, dibutyryl-cyclic AMP and theophylline.

There is evidence that the relaxation of vascular smooth muscle produced by isoproterenol or cyclic AMP is mediated by membrane hyperpolarization. The current study investigates the possibility that this hyperpolarization, and hence the relaxation, may be produced by activation of the electrogenic sodium pump. Rat and pig tail artery strips were placed in a 1.0-mM potassium solution for 15 min. This procedure results in a decrease in the activity of the sodium pump. The strips were then made to contract in response to norepinephrine. Two minutes later, the concentration of potassium was increased to 6.0 mM and a relaxation occurred. The amplitude of this relaxation reflects the activity of the sodium pump. Either isoproterenol or dibutyryl-cyclic AMP causes an enhancement (time or degree) of potassium-induced relaxation. Theophylline potentiated potassium-induced relaxation in pig arteries but not in rat arteries. The relaxant action of isoproterenol on 1.0 mM barium contractures of rat arteries was inhibited by treatment with ouabain or with potassium-free solution. Ouabain inhibited the relaxant action of isoproterenol in pig arteries contracted with depolarizing potassium solution but not in rat tail arteries. Dibutyryl-cyclic AMP, theophylline and nitroprusside caused relaxation of serotonin-induced contractions; however, in rat arteries these responses were not inhibited by ouabain or by the absence of potassium. Similar studies on tail arteries from baboons, dogs, pigs and cats showed that relaxation by dibutyryl-cyclic AMP or by theophylline had some dependency on the activity of the sodium pump. These observations are consistent with the following conclusions: 1) isoproterenol and cyclic AMP potentiate the electrogenic pumping of sodium and potassium responsible for potassium-induced relaxation; 2) the relaxing action of isoproterenol, dibutyryl-cyclic AMP and theophylline are dependent upon experimental conditions and the species from which the vascular tissue is obtained; and 3) there is a component of isoproterenol- and cyclic AMP-induced relaxation which is not altered by inhibition of the electrogenic sodium pump in the rat.

Animals↗
PubMed1981

Calcium antagonism is no rose.

Much remains to be defined about the mechanism of action of calcium entry blockers. The diversity of their pharmacological actions reflects the many effects of the calcium ions which they block. The observation that D-600 decreases myogenic tone in the rabbit basilar artery, whereas it increases this tone in the facial vein, is cited as an example of this diversity.

Animals↗
PubMed1981

Different behavior of the resistance vessels of the human calf and forearm during contralateral isometric exercise, mental stress, and abnormal respiratory movements.

Experiments were conducted in normal human volunteers to compare the response of the forearm and calf vessels to contralateral isometric exercise, mental stress, resisted breathing, coughing, and the Valsalva maneuver. Blood flows were measured by means of strain-gauge plethysmography, arterial blood pressure by auscultation, and heart rate by electrocardiography. Isometric exercise of one forearm (at one-third maximal voluntary contraction) for 90 seconds caused an increase in blood pressure and heart rate; the vascular resistance decreased in the resting forearm, and increased in the calf. The decrease in forearm resistance was greater with the subjects supine and attenuated with the subjects standing or reclining head-down. With arterial occlusion of the exercising forearm just prior to cessation of the handgrip, the blood pressure and the calf resistance remained elevated, while the heart rate returned to control. The forearm resistance increased during the occlusion period and remained elevated throughout it. Mental stress caused an increase in heart rate and blood pressure and a dilation of the forearm but not of the calf vessels; these changes were smaller in standing than in supine subjects. Resisted breathing and coughing caused an increase in heart rate and in forearm blood flow, but not in calf blood flow. The Valsalva maneuver was followed by decreases in blood flow to the upper and lower limbs. The different responses in forearm and calf vessels can be explained by a central component which triggers a vasodilator pathway (possibly cholinergic) which is distributed to forearm but not to calf vessels.

Adult↗
PubMed1981

Cocaine and contractile responses of vascular smooth muscle from spontaneously hypertensive rats.

The goal of this study was to compare the effects of cocaine on contractile responses of isolated vascular smooth muscle from spontaneously hypertensive (SHR) and normotensive rats. Helical strips of tail artery from adult SHR and normotensive rats were mounted in organ chambers between two platinum wire electrodes; isometric contractions were recorded. Vascular responsiveness was determined before and after acute denervation with 6-hydroxydopamine or before and after treatment with cocaine. Cumulative addition of cocaine (10(-10) to 10(-3)M) produced contraction of the strips. SHR was found to be les sensitive to cocaine than normotensive rats. Contractions induced by cocaine were blocked by phentolamine and reduced after acute denervation. The sensitivity to exogenous norepinephrine (3 X 10(-12) to 3 X 10(-5)M) and contractile responses to electrical stimulation (0.1 to 16 Hz) of innervated strips were similar for SHR and normotensive rats. Cocaine (10(-6)M) potentiated contractile responses to norepinephrine and electrical stimulation. The magnitude of potentiation to norepinephrine and to electrical stimulation was greater in SHR than in normotensive rats. Cocaine (10(-6) M) produced relaxation of strips contracted with tyramine (10(-4) M). The magnitude of relaxation induced by cocaine was less in SHR than in normotensive rats. The uptake of 3H-norepinephrine was greater in tail arteries isolated from SHR as compared to those from normotensive rats. Cocaine (10(-4)M) inhibited the uptake of 3H-norepinephrine in both groups of rats. The magnitude of inhibition was greater in SHR. These results suggest that the neuronal uptake pump in blood vessels from SHR is more efficient than that in normotensive rats.

Animals↗
PubMed1980

Vascular reactivity in hypertension: altered effect of ouabain.

Ouabain inhibits the relaxing effect of Ca2+ (but not of Mn2+) on contractile responses in tail artery strips isolated from spontaneously hypertensive and normotensive rats. The magnitude of ouabain inhibition was greater in vascular strips from hypertensive rats suggesting a significant difference in basic membrane function in hypertensive vascular smooth muscle.

Animals↗
PubMed1980

Pre- and post-junctional adrenergic mechanisms and hypertension.

1. The ability of the blood vessel wall to synthesize noradrenaline is augmented at the early stages of genetic hypertension in animals. It usually is normal, or reduced in chronic hypertension. 2. The exocytotic release of noradrenaline is greater than normal, in the early stages of a number of experimental models of hypertension. 3. Postjunctional receptors for noradrenaline are not uniform throughout the vascular tree. Their sensitivity changes during the development of high blood pressure. 4. In chronic hypertension neuronal uptake and the extraneuronal disposition of released noradrenaline is depressed in the heart, but accelerated in the blood vessel wall. 5. The adrenergic neuro-effector interaction undergoes a diverging long-term adaptation in the heart and the blood vessels of hypertensive animals. In the former this tends to increase, but in the latter to reduce, the efficiency of sympathetic nervous control.

Angiotensin II↗
PubMed1980

Inactivation of released norepinephrine in rat tail artery by neuronal uptake.

The relationship between adrenergic nerve activity and neuronal uptake was investigated. Helically cut strips of rat tail artery were mounted in organ chambers and isometric contractions were recorded. Spontaneous contractions were occasionally observed and these contractions were blocked by phentolamine. Cumulative addition of cocaine produced contractions of the strips. These contractions were blocked by phentolamine and reduced after denervation with 6-hydroxydopamine. Cocaine potentiated the contractile responses to exogenous norepinephrine and caused a shift to the left in the concentration--response curve. Contractions in response to low-frequency field stimulation were potentiated by cocaine; contractions produced by high frequencies were not altered by the drug. Cocaine had no effect on contractions produced by depolarization of the prejunctional membrane with high potassium. The relative rates of relaxation following high- and low-frequency stimulation were increased similarly by cocaine. The results indicate (1) the spontaneous activity of rat tail artery is related to the leakage of norepinephrine from nerve endings; (2) contraction in response to cocaine alone probably results from inhibition of neuronal uptake and the release of endogenous norepinephrine; and (3) the amine uptake mechanism is not operative during depolarization of prejunctional membrane.

Animals↗
PubMed1980

Prostaglandins and potassium relaxation in vascular smooth muscle of the rat. The role of Na-K ATPase.

We explored the hypothesis that postaglandin-induced vasodilation is caused by activation of the electrogenic sodium-potassium pump which results in membrane hyperpolarization and relaxation of vascular smooth muscle. Helical strips of rat tail artery relax in response to potassium after norepinephrine-induced contractions in physiological salt solution containing a low-potassium concentration. The amplitude of this potassium relaxation is used as an index of sodium-potassium ATPase activity. It was observed that PGA1, PGE2, and PGF2alpha (10(-6) g/ml) significantly enhanced the magnitut. PGE2 caused relaxation of contractions induced by either 25 mM KCl or norepinephrine (10(-9) g/ml), and these relaxations were inhibited by 10(-4) M ouabain. Indomethacin (5.3 x 10(-6) g/ml) and meclofenamate (10(-6) g/ml) reduced the magnitude of potassium-induced relaxation by more than 30% of control. PGF2alpha (10(-5) g/ml) reversed the inhibition of potassium relaxation by meclofenamate. These observations suggest that prostaglandins induce vascular smooth muscle relaxation by stimulation of the sodium pump and that endogenous prostaglandins normally potassium relaxation.

Animals↗
PubMed1979

Skeletal muscle capillary densities during reactive hyperemia.

Reactive hyperemia was induced in hindlimbs of rats by occlusion of the femoral artery. Using fluorescein dye as a peripheral vascular marker, we observed that there was an increase in the number of flowing capillaries supplying the muscle fibres following release of the occlusion. The results indicate that the number of flowing capillaries is not dependent on the duration of occlusion (2-10 min).

Animals↗
PubMed1979

In vitro effects of desoxycorticosterone on vascular smooth muscle.

We present evidence in accord with the observations of S. Kalsner (Br. J. Pharmacol. 36: 582-593, 1969) that in the rabbit aorta, desoxycorticosterone (DOC) potentiates the contractile response to certain catecholamines by inhibiting their degradation by catechol-O-methyltransferase. In contrast, DOC depresses the contractile responses in rat aorta and tail arteries. To elucidate the mechanism of this depression the effect of DOC was evaluated under various conditions. DOC depressed the contractile response to epinephrine, phenylephrine, KCl, and angiotensin II. The depression was unaltered by ouabain or by a potassium-free solution, indicating that DOC did not produce its depression by altering Na-K-ATPase activity. The depression is unaltered in a chloride-free solution, demonstrating that the DOC effect is not caused by a change in membrane permeability to chloride. Radioisotope studies demonstrate that DOC does not alter membrane permeability to potassium. Removal of extracellular calcium with EGTA (ethylene glycol-bis (beta-aminoethyl ether) N, N'-tetraacetic acid) significantly reduced the magnitude of the DOC depression. Indirect evidence is presented suggesting that DOC might increase calcium binding to the plasma membrane, resulting in its stabilization and hence in a depression of the contractile response.

Angiotensin II↗
PubMed1979

Potassium relaxation of vascular smooth muscle from spontaneously hypertensive rats.

Helical strips of tail artery from spontaneously hypertensive (SHR) and Kyoto Wistar normotensive rats (WKY) were observed to relax in response to potassium after contraction induced by norepinephrine in potassium-free solution. Helical strips from SHR consistently showed greater relaxation in response to the addition of potassium than did those from WKY. The amplitude of potassium-induced relaxation is believed to be an index of the activity of electrogenic sodium-potassium transport and hence of sodium-potassium ATPase. Thus, the sodium-potassium ATPase activity of SHR vascular smooth muscle is increased as compared to WKY. This interpretation is supported by the observation that ouabain eliminated potassium-induced relaxation in both SHR and WKY strips. Potassium-induced relaxation in SHR was more sensitive to ouabain inhibition than in WKY. Relaxation induced by potassium in SHR and WKY strips was also shown to vary with: (1) the length of incubation in potassium-free solution, and (2) the concentration of potassium added back. The results of these experiments on potassium-induced relaxation serve as evidence that SHR have either an increased intrinsic sodium-potassium ATPase activity, or an enzyme activity that has been stimulated to a greater degree by an elevated intracellular sodium concentration which resulted from the incubation in potassium-free solution.

Animals↗
PubMed1979

Prescribing in Australia. Part 2.

A brief history of the Australian Pharmaceutical Benefits Scheme is given. Available statistics in recent years have been analyzed indicating the more frequently prescribed drugs both individually and in the major pharmacological groups. Part 1, which covers antibiotics and analgesics was published in AFP, February, 1979.

Administration, Topical↗
PubMed1979

Prescribing in Australia. Part 1.

A brief history of the Australian Pharmaceutical Benefits Scheme is given. Available statistics in recent years have been analyzed indicating the more frequently prescribed drugs both individually and in the major pharmacological groups.

Analgesics↗