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Biomedical subjects

M G Salom

Publications and source records attributed to M G Salom.

24 records · Page 2Linked to original sources

Blood pressure control in pithed rat.

In the pithed Wistar rats Captopril (2 mg/kg) decreased the mean arterial pressure (MAP) 21%. Further injection of a specific antagonist decreased the vasoconstrictor action of vasopressin (aAVP, 10 micrograms/kg) an additional 6%. Reversal in the order of drug administration did not change these percentages. The osmotic stimulus evoked by the infusion of hypertonic saline (ClNa 9%, 0.018 ml/min, 2 hr) significantly increased MAP, this increase being almost totally reversed by the aAVP (10 micrograms/kg). These findings suggest a greater role of the renin-angiotensin system than of the vasopressin (AVP) in the maintenance of MAP in the pithed rat; AVP, moreover, can be released by means of an osmotic stimulus.

Animals↗

Sympathoadrenal activity and plasma glucose effects on plasma dopamine-beta-hydroxylase levels in rats.

Plasma dopamine-beta-hydroxylase (DBH) activity is a controversial index of sympathoadrenal function. In our results, the half-life of bovine DBH administered by cardiac puncture to Wistar rats was dependent on plasma glucose values, being 60 min for controls, 96 min for streptozotocin (STZ)-diabetic animals (p less than 0.02) and 33 min for insulin-treated normal rats (p less than 0.01). In experimental situations with low plasma glucose levels, DBH activity was also diminished with respect to controls (glucose: 103.6 +/- 2.2 mg%, DBH: 9.7 +/- 0.5 U/ml). After fasting, glucose was 60.8 +/- 1.5 mg% (p less than 0.001) and plasma DBH 6.4 +/- 0.3 U/ml (p less than 0.001); fasting plus cold exposure also decreased glucose (66.2 +/- 1.4 mg%, p less than 0.001) and plasma DBH (6.7 +/- 0.2 U/ml; p less than 0.001). In both situations, there was an increase in exocytosis from sympathoadrenal tissues; however, no increase in plasma DBH levels was observed, because plasma glucose being diminished it was unable to compete at the catabolic receptor level. When normal plasma glucose levels take place, plasma DBH is essentially constant, poorly reflecting a moderate increase or decrease in exocytosis from tissues, as was the case in our animals with 48 h of cold exposure. When chemical sympathectomy (6-OH-dopamine) or bilateral adrenalectomy was performed there was a compensatory mechanism between them. Plasma DBH does not change significantly in these situations if plasma glucose values are normal. From these results, the most important physiological influence on plasma DBH activity is the glucose plasma levels. Plasma DBH values not being a useful index of sympathoadrenal activity if, at the same time, the plasma glucose levels are not considered.

Adrenal Glands↗

Effect of captopril on norepinephrine vascular contractility.

In isolated aortic rings and in vitro perfused mesenteric arteries of Wistar rats the vasoconstrictor responses to norepinephrine (NE) were not affected by captopril (2 X 10(-4) M). However, captopril (1 mg/kg i.v.) in pithed Wistar rats attenuated significantly the increases in diastolic blood pressure induced by NE. In pithed rats the effect of captopril on NE diastolic blood pressure responses disappeared either in the presence of an angiotensin II (5 ng X kg-1 X min) infusion or when the rats were previously nephrectomized. These findings suggest that the effect of captopril on vascular responses to norepinephrine is mediated by an inhibition of the renin-angiotensin system and not by an antagonistic effect on alpha-adrenergic receptors.

Angiotensin II↗

Role of sodium balance on maintenance of blood pressure in the chronic phase of two-kidney, one-clip hypertension.

Blood pressure and sodium balance have been studied after unclipping, nephrectomy and sham operation of ischemic kidney in the chronic phase (16 weeks) of two-kidney, one clip hypertension. In hypertensive rats the fractional excretion of sodium was 85.5 +/- 2.3% and blood pressure (BP) was significantly increased (187.1 +/- 4.5 mmHg, p less than 0.001). Removal of either the constricting clip or ischemic kidney induced a decrease of BP to normal level whereas sham operation did not produce any change. However, rats submitted to these three experimental manipulations showed, at 1, 2, 3 and 4 days, and at 3 weeks, similar changes in sodium excretion. In the groups with unclipping or nephrectomy of ischemic kidney, water intake was less and urine volume smaller than in the sham operated group. These results suggest that a positive sodium balance is not important to maintain hypertension at this stage and that changes in sodium balance, after both unclipping and nephrectomy of ischemic kidney, have no influence in BP normalization.

Animals↗

Normal hemodynamic parameters in conscious Wistar rats.

The evolution of different hemodynamic parameters with ponderal growth has been studied in conscious Wistar rats. The thermodilution method has been used to determine cardiac output and related variables. The results suggest that, between animal weight and the different hemodynamic parameters, there is a direct proportional relationship to blood volume, mean arterial pressure, cardiac output, stroke volume and total peripheral resistance, and an indirect proportional relationship to heart rate, cardiac index and stroke volume index. Body weight, therefore, plays a major role in hemodynamic determination, this having to be kept in mind when designing the experiment.

Animals↗

Role of renin-angiotensin and sympathetic nervous systems in the chronic phase of two-kidney, one-clip hypertension in rats.

The purpose of the present study was to examine the role of the renin-angiotensin and the sympathetic nervous systems during the chronic phase (greater than 16 weeks) of two-kidney, one-clip hypertension in conscious unrestrained rats. During this phase, the mean arterial pressure (MAP) (p less than 0.001) and plasma angiotensin II (31.9 +/- 1.5 to 125.8 +/- 19.9 pg/ml, p less than 0.005) were significantly increased as compared to normotensive group. Converting enzyme inhibition by captopril produced a significant decrease of MAP (181.2 +/- 8.2 to 140.0 +/- 5.5 mmHg, p less than 0.001). This hypotensive response was similar when aprotinin (a Kallikrein inhibitor) and captopril were infused simultaneously. Alpha 1-adrenergic receptor blockade by phenoxybenzamine (POB) significantly decreased but did not normalize MAP (179.8 +/- 12.4 to 135.8 +/- 10.4 mmHg, p less than 0.001). However, when infused after POB, captopril induced a further decrease of MAP to 86.7 +/- 9.4 mmHg (p less than 0.001). This MAP level was not different from that found in normotensive rats after infusion of the two drugs (83.2 +/- 5.3 mmHg). These results suggest that both the renin-angiotensin system and the sympathetic nervous system, by activating peripheral alpha 1-adrenergic receptors, maintain the high blood pressure during the chronic phase (greater than 16 weeks) of two-kidney, one-clip hypertension in conscious rats.

Angiotensin II↗