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M C Sutter

Publications and source records attributed to M C Sutter.

33 records · Page 2Linked 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↗
PubMed1977

Contractile responses to noradrenaline: varying dependence on external calcium of consecutive vascular segments of perfused rat hindquarters.

To study the dependency of vascular smooth muscle contractions, produced by noradrenaline, on the concentration of extracellular calcium, experiments were performed on adult male Wistar rats. The hemodynamic characteristics of the isolated, perfused hindquarters were investigated from maximal dilatation up to maximal, noradrenaline-induced constriction under constant flow conditions. Pressor responses to noradrenaline in the consecutive segments of the vascular bed ("proximal" and "distal" precapillary resistance vessels and postcapillary resistance vessels) were determined at low (0.2mM) and at normal (1.5-2.0 mM) Ca++ concentrations in the perfusate. Dependence on external calcium is much greater peripherally. The smallest pre- and postcapillary resistance vessels are the most dependent while the larger, "proximal" resistance vessels are the least dependent on the availability of external calcium. The results illustrate the considerable differentiation of smooth muscle, depending on its location along the vascular circuit. They further indicate that it is likely that the hemodynamically so important microvessels are highly dependent on extrinsic Ca++ sources not only concerning their involvement of remote adrenergic control, but also in their maintenance of normally pronounced "myogenic" tone.

Animals↗
PubMed1977

Contractility, muscle mass and agonist sensitivity of isolated portal veins from normo- and hypertensive rats.

Properties of the longitudinal smooth muscle of portal veins from normotensive Wistar rats, adult (NCR) and young (NCRy); spontaneously hypertensive Okamoto rats, adult (SHR) and young (SHRy); and adult Wistar rats with renal hypertension (RHR) were studied in vitro and histologically. Some aortic strips from SHR and SHRy were compared with controls. In response to noradrenaline (NA) and acetylcholine (ACh) greater maximum force was developed by veins from all hypertensive groups than by those from control rats. Cross-sectional area of the longitudinal muscle of veins from SHR but nor SHRy nor RHR was greater than control. Maximum stress in response to agonists was greater in both SHR and RHR than NCR. ED50-values for NA and ACh were lower in portal veins from SHR than NCR but not from RHR nor SHRy compared to controls. Denervation did not abolish any of the differences between SHR and NCR. Aortic strips from SHR developed less maximum force to NA and ED50 was greater than those from NCR, i.e. opposite to the findings in portal veins. Low levels of external Ca2+ reveal altered calcium handling in veins from SHR compared to controls. It is concluded that portal veins from hypertensive rats are functionally different from those of normotensive rats and differ in SHR compared to RHR. It is suggested that the altered functional properties of portal vein, but not of aorta, in several respects resemble those of arterial resistance vessels. The implications of these findings are discussed in terms of mechanisms of hypertension in these animal models.

Acetylcholine↗
PubMed1975

Quantitative aspects of cyclic AMP and relaxation in the rabbit anterior mesenteric-portal vein.

Rabbit anterior mesenteric-portal vein was shown to exhibit a positive correlation between relaxation and cyclic AMP levels using different concentrations of isoproterenol for varying exposure times. No consistent relationship was found between cyclic AMP and relaxation using a series of phosphodiesterase inhibitors (papaverine, SC2964, or RA233). In sodium-free (Tris-substituted) Kreb's solution, the addition of isoproterenol still increased cyclic AMP levels, but there was no relaxation. Dibutyryl cyclic AMP was also ineffective in sodium-free solution. Under identical conditions, both relaxation and increases in cyclic AMP produced by papaverine and SC2964 were found to be independent of extracellular sodium. We conclude, therefore, that increased cyclic AMP may be involved in isoproterenol-induced relaxation possibly acting via increased Na+-Ca2+ exchange, but plays only a small role, if any, in smooth muscle relaxation produced by papaverine, RA233, or SC2964.

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↗
PubMedDate not supplied

Chronic ethanol consumption, stress, and hypertension.

A reliable method of producing physical stress in the rat was developed using heat irradiation, and the possible interaction between chronic ethanol consumption and stress was investigated in a rat model of alcoholism. Chronic heat stress and chronic ethanol consumption each produced mild hypertension in rats. When combined, the two treatments resulted in hypertension more severe than that produced by either stress or ethanol consumption alone. The group of animals receiving both treatments also exhibited high mortality. Investigations into the mechanisms responsible for the apparent additive effects of the two treatments revealed that the animals in this group had the highest circulating norepinephrine levels. The plasma volumes, however, were not different between the stressed groups and their unstressed counterparts. As the plasma norepinephrine level usually reflects overall sympathetic tone of an animal, our results suggest that the additional hypertensive effect of chronic stress on the ethanol-treated animals is associated with increased sympathetic nervous activity and is not a result of expanded plasma volume. These findings may have clinical implications for human alcoholics and in the analysis of cardiovascular risk factors in hypertensive patients.

Alcoholism↗