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Biomedical subjects

C C Pang

Publications and source records attributed to C C Pang.

99 records · Page 6Linked to original sources
PubMed1980

Contractile responses of aortic and portal vein strips during the development of DOCA/salt hypertension.

Vascular smooth muscle strips were examined during the development of hypertension in rats treated with deoxycorticosterone acetate (DOCA) plus saline to determine if the changes in the contractile responses precede or succeed the increase in blood pressure. After treatment with DOCA/salt for 1, 3 and 4 weeks, aortic and portal vein strips were prepared from control and treated rats for studies of cumulative dose-response relationships to noradrenaline (NA) in Krebs' solutions containing normal (2.5 mM) or low (0.2 and 0.4 mM) concentrations of Ca. 1 week of treatment did not result in any change in blood pressure or in the stress (force/area) developed by the aortic strips in response to NA in normal or low Ca. 3 weeks of treatment caused a significant increase of pressure and the aortic strips developed a significant decrease of stress in response to NA in normal, but not in low Ca. 4 weeks of treatment resulted in a significant increase of pressure and a significant decrease of stress in response to NA in low, as well as in normal, Ca. In contrast to the aortic strips, there was no change in the force induced by NA in the portal vein strips at any time. Thus, the decrease of contractile response in the aortic strips during treatment with DOCA/salt followed the same time course as the increase of arterial pressure and may be a consequence of high blood pressure.

Animals↗
PubMed1980

Hydralazine prevents changes in the contractile response of aortic but not portal vein strips in hypertensive rats.

Previous studies showed that aortic strips from rats with either spontaneous (SHR) or DOCA/salt-induced hypertension developed less stress (force/area) in response to noradrenaline (NA) when compared to aortic strips from normotensive rats. Portal vein strips from SHR, but not from DOCA/salt hypertensive rats, developed greater force to NA compared to strips from control rats. We have investigated whether these changes are prevented by hydralazine. Hydralazine was added to the drinking solution (1% NAC1) of one group of rats from the first day of treatment with DOCA. In the second group, hydralazine was added to the drinking water of 13-week-old SHR. After 3 weeks of treatment with hydralazine, cumulative dose-response relationships to NA were studied using aortic and portal vein strips from hydralazine-treated and control rats. Hydralazine prevented the increase of arterial pressure and the decrease of stress developed to NA by the aortic strips from both SHR and DOCA/salt rats. It did not prevent the increase of force developed to NA by the portal vein strips from SHR. Thus, reduced contractile response of the aortic strips from hypertensive rats seems to be the result of a high pressure, since both the rise in blood pressure and reduced aortic response are prevented by hydralazine. Increased contratile response of the portal vein strips from SHR appears to be independent of blood pressure.

Animals↗
PubMed1979

Hypophysectomy and saralasin on mesenteric vasoconstrictor response to vasopressin.

The dose-response relationship of the mesenteric resistance vessels to vasopressin was studied in anesthetized laparotomized cats before and after hypophysectomy and again during the plateau phase of the response to a prolonged infusion of [Sar1-Ala8] angiotensin II (saralasin), a competitive antagonist of angiotensin II. Hypophysectomy and saralasin each caused an increase in superior mesenteric arterial conductance. Before hypophysectomy infusion of 0.5 mU/(min.kg) of vasopressin caused mesenteric conductance to decrease from 0.168 to 0.156 ml/(min.kg.mmHg), a change of only 0.012 units. After hypophysectomy, the same dose reduced conductance from 0.227 to 0.179 mU/(min.kg.mmHg), a change of 0.048 units. During the plateau phase of the response to saralasin, 0.5 mU/(min.kg) of vasopressin reduced conductance from 0.281 to 0.201 ml/(min.kg.mmHg), a change of 0.079 units. Hypophysectomy and saralasin had little effect on the mesenteric vasoconstrictor response to high doses of vasopressin (2.0-10 mU/(min.kg). The ineffectiveness of low doses of vasopressin on the mesenteric resistance vessels of the intact anesthetized, surgically stressed animal may be due in part to the already constricted state of the bed caused by endogenous vasopressin and angiotensin and in part due to an opposing vasodilator influence, the reflex withdrawal of the vasoconstrictor effect of endogenous vasopressin.

Angiotensin II↗
PubMed1977

Vasopressin and angiotensin: reciprocal mechanisms controlling mesenteric conductance.

Intravenous infusions of [Sar1-Ala8]angiotensin II, acute hypophysectomy, and acute intestinal denervation were carried out in 15 pentobarbital-anesthetized cats. Infusion of the angiotensin II antagonist caused only a small increase in superior mesenteric arterial conductance and a small decrease in arterial pressure in intact animals, but the changes were subypophysectomy alone caused only a small intestinal vasodilatation and little change in arterial pressure. However, the responses to hypophysectomy were much larger when the gland was removed during a prolonged infusion of the angiotensin II antagonist. Intestinal denervation caused only minor changes in mesenteric conductance and arterial pressure, and the responses to [Sar1-Ala8]angiotensin II and hypophysectomy were largely unaltered by the presence or absence of the intestinal innervation. The results suggest that the renin-angiotensin and vasopressin systems are reciprocal overlapping mechanisms that exert a significant vasoconstrictor influence on the intestinal resistance vessels in the anesthetized cat. In the absence of one control system, the other appears to compensate to maintain resistance.

Angiotensin II↗
PubMedDate not supplied

Autonomic control of the venous system in health and disease: effects of drugs.

The venous system contains approximately 70% of the blood volume. The sympathetic nervous system is by far the most important vasopressor system in the control of venous capacitance. The baroreflex system responds to acute hypotension by concurrently increasing sympathetic tone to resistance, as well as capacitance vessels, to increase blood pressure and venous return, respectively. Studies in experimental animals have shown that interference of sympathetic activity by an alpha1- or alpha2-adrenoceptor antagonist or a ganglionic blocker reduces mean circulatory filling pressure and venous resistance and increases unstressed volume. An alpha1- or alpha2-adrenoceptor agonist, on the other hand, increases mean circulatory filling pressure and venous resistance and reduces unstressed volume. In humans, drugs that interfere with sympathetic tone can cause the pooling of blood in limb as well as splanchnic veins; the reduction of cardiac output; and orthostatic intolerance. Other perturbations that can cause postural hypotension include autonomic failure, as in dysautonomia, diabetes mellitus, and vasovagal syncope; increased venous compliance, as in hemodialysis; and reduced blood volume, as with space flight and prolonged bed rest. Several alpha-adrenoceptor agonists are used to increase venous return in orthostatic intolerance; however, there is insufficient data to show that these drugs are more efficacious than placebo. Clearly, more basic science and clinical studies are needed to increase our knowledge and understanding of the venous system.

Aging↗
PubMedDate not supplied

Measurement of body venous tone.

The venous system contains about 70% of the blood volume, and approximately 75% of the venous volume is in the small veins and venules. Veins play an active role in the control of cardiac output (CO) and blood pressure. Drugs that interfere with venous tone have profound effects on CO and blood pressure due to the large venous capacity. Information on body venous tone cannot be obtained from studies using isolated venous preparations and perfused venous beds, which lack modulating cardiovascular reflex mechanisms. In vivo methods used for the assessment of venous function in experimental animals and humans are as follows: the mean circulatory filling pressure (MCFP) method for the determination of body venous tone, constant CO reservoir technique for measuring vascular compliance and unstressed volume, plethysmography or blood-pool scintigraphy along with venous occlusion for measuring the volume and compliance of an organ, linear variable differential transformer (LVDT) technique for estimating the diameter of a human dorsal hand vein, intravascular ultrasound (IVUS) imaging technique to monitor the cross-sectional area of a large vein, and ultrasonic crystals to estimate the dimension of an organ. These methods are described and critically evaluated to disclose their validity, merits and limitations.

Animals↗
PubMedDate not supplied

Effect of chronic treatment of spontaneously hypertensive rats with D 600.

The effects of chronic treatment of spontaneously hypertensive rats (SHR) with methoxyverapamil (D 600) on blood pressure (BP) and on the in vitro contractile response of aortic and portal vein strips of rats were examined. D 600, prepared as the free base and dissolved in sesame oil, was injected subcutaneously daily into SHR to maintain the systolic blood pressure (SBP) at less than 130 mm Hg for 24 hours after injections. The dose required increased progressively from 4 to 8.5 mg/day/rat. As controls, normotensive rats (WKY) and untreated SHR received daily injections of the vehicle. After 2 weeks, aortic and portal vein strips were prepared from each rat for studies of cumulative dose-response curves to norepinephrine (NE) in Krebs' solution containing normal (2.5 mM) and low (0.2 and 0.4 mM) calcium (Ca). Chronic treatment with D 600 restored to control values the ordinarily depressed contractile response to NE and increased the ED50 values for NE (i.e., the NE dose that produces 50% of the maximum response) of aortic strips from SHR in nord-mal and low Ca. Portal veins from SHR showed increased spontaneous activity, supernormal responses to NE, and decreased ED50 values for NE that were all exaggerated by chronic D 600 treatment. These results imply that SHR developed a tolerance to D 600 associated with enhanced contractility of vascular smooth muscles.

Animals↗