Search PubMed⌕ Search

Biomedical subjects

H C Salgado

Publications and source records attributed to H C Salgado.

54 records · Page 3Linked to original sources
PubMed1988

Extent of baroreceptor resetting in response to sodium nitroprusside and verapamil.

We investigated the effect of sodium nitroprusside, verapamil, and hemorrhage on the resetting of the aortic baroreceptors of normotensive control rats to hypotension, and the reversal of resetting of baroreceptors of one-kidney, one clip hypertensive rats to normotension. Using whole-nerve recording, the extent (%) of resetting (or reversal of resetting) observed 15 minutes after a maintained fall in mean arterial pressure (MAP) was evaluated by the ratio between changes of systolic threshold pressure for baroreceptor activation and changes of control diastolic pressure exhibited by the rats, multiplied by 100. Three groups of normotensive control rats showed a MAP decrease to hypotensive levels of 33%, 39%, and 41%, respectively, with sodium nitroprusside, verapamil, and hemorrhage. The corresponding extent of resetting was 96 +/- 3%, 39 +/- 2%, and 46 +/- 4%, respectively. Only in the group treated with verapamil did MAP and systolic threshold pressure not revert completely to normotensive levels 15 minutes after the end of drug infusion. Three groups of one-kidney, one clip hypertensive rats showed MAP normalization of 30%, 37%, and 31%, respectively, with sodium nitroprusside, verapamil, and hemorrhage. The corresponding extent of reversal of resetting to normotension was 107 +/- 3%, 40 +/- 2%, and 60 +/- 9%, respectively. Again, only in the group treated with verapamil did MAP and systolic threshold pressure not revert to hypertensive levels 15 minutes after infusion. Besides indicating that different vasodilators can differently modulate the rapid (15-minute) resetting (or reversal of the resetting) due to similarly maintained fall in MAP, these data suggest that verapamil has a nonspecific effect on the baroreceptors, whereas sodium nitroprusside appears to affect baroreceptor transduction.

Animals↗
PubMed1987

Changes of the intrinsic heart rate during the onset of renal hypertension.

Intrinsic heart rate (IHR) measured after autonomic blockade with atropine and propranolol in conscious one-kidney, one clip (1-K,1C) hypertensive rats was increased and associated with the peak of tachycardia that occurs 7 days after clipping. No significant changes in basal or intrinsic heart rate were observed 3 or 14 days after clipping. The effect of exogenous angiotensin II (ANG II) was compared to that of norepinephrine (NOR) and isoproterenol (ISO) in conscious normotensive rats. Infusion of ANG II for 3 h induced a slight increase in heart rate which was accompanied by a larger increase in IHR. In contrast, the infusion of NOR or ISO induced intense tachycardia without affecting IHR. The intense tachycardia observed in conscious rats 48 h after sinoaortic denervation, was not accompanied by changes in IHR. Furthermore, the adrenergic stimulation produced by infusion of either NOR or ISO or that occurring after 48 h of sinoaortic denervation, did not modify IHR in conscious rats, whereas a 3-h infusion of ANG II did. These data suggest that the tachycardia observed in rats during the onset of 1-K,1C hypertension may be partly due to increased IHR caused by ANG II.

Angiotensin II↗
PubMed1986

Effect of DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid on the blood pressure response to vasoactive substances.

The importance of kininase I (carboxypeptidase N) in the catabolism of circulating kinins is not known. DL-2-Mercaptomethyl-3-guanidinoethylthiopropanoic acid (MGTA) has been reported to be an inhibitor of kininase I both in vitro and in vivo. In order to evaluate the possible role of kininase I in the in vivo inactivation of bradykinin, the authors studied the blood pressure responses of pentobarbital-anesthetized rats to bradykinin before and after the i.v. administration of MGTA (a 10-mg/kg bolus followed by 1 mg/kg/min continuous infusion). MGTA potentiated bradykinin-induced hypotension. The specificity of MGTA for kininase I was tested using other peptide and nonpeptide vasoactive substances. MGTA potentiated the hypertension due to angiotensin I, angiotensin II and vasopressin, but it did not affect the response to phenylephrine. On the other hand, MGTA did not potentiate the hypotensive action of acetylcholine, but it did potentiate that of sodium nitroprusside. The potentiation of bradykinin-induced hypotension is compatible with inhibition of kininase I by MGTA. The data suggest, however, that MGTA is not selective for any enzyme that inactivates kinins, inasmuch as other peptides and nonpeptide vasoactive substances are also potentiated.

3-Mercaptopropionic Acid↗
PubMed1986

Cardiovascular reflexes in conscious sodium-depleted rats.

Reflex arterial pressure regulation was studied in control and sodium-depleted rats fed a diet containing 0.1 mEq Na+ for 6 days associated with furosemide (5 mg/kg, ip, on the 1st and 5th day). The hypertensive response produced in conscious rats by bilateral common carotid occlusion (5 to 60 s) was significantly smaller in the sodium-depleted rats (MAP = 113 +/- 3 mmHg) than in the controls (MAP = 121 +/- 2 mmHg) in terms of absolute as well as relative values. Sixty min after recovery from ether anesthesia, the rats submitted to sino-aortic denervation showed a similar relative increase in MAP (30%), whereas the hypertensive level attained by the sodium-depleted rats was only mild (MAP = 126 +/- 5 mmHg). Sodium-depleted rats required 3.5 and 2.4 times larger dose of norepinephrine and angiotensin II, respectively, than the control rats to produce an increase in MAP of 20-25 mmHg. Changes in vascular reactivity associated with impaired cardiac function might be important factors to explain the decreased pressor responses produced by carotid occlusion and by sino-aortic denervation in sodium-depleted rats.

Angiotensin II↗
PubMed1985

Hemodynamics and sodium balance in conscious sodium-depleted rats.

The objective of this paper was to study the hemodynamics (mean arterial pressure, cardiac output, total peripheral resistance, stroke volume and heart rate) of conscious rats submitted to 6 days of sodium depletion. Sodium balance of sodium-depleted rats on a low-sodium diet (0.1 mEq/day) associated with furosemide (10 mg/kg, ip on the first and fifth day) for 6 days indicated that the animals were studied under a negative sodium balance on the sixth day. The overactivity of the renin-angiotensin system in sodium-depleted rats was demonstrated by the fall in mean arterial pressure (15 +/- 2 vs 0.5 +/- 1 mmHg in sodium-depleted and control rats, respectively), after blocking the converting enzyme with BPP9a (SQ 20881) and also by evaluating plasma renin activity (10 +/- 8 vs 3.0 +/- 0.6 ng AI ml-1 h-1 in sodium-depleted and control rats, respectively). Thermodilution measurements showed that the cardiac output of sodium-depleted animals was reduced by 35% (29 +/- 2 vs 45 +/- 4 ml min-1 100 g-1 for sodium-depleted and control rats, respectively), with partial compensation by a 37% increase in total peripheral resistance (3.7 +/- 0.3 vs 2.7 +/- 0.2 PRU for sodium-depleted and control rats, respectively), resulting in an 11% decrease in mean arterial pressure (104 +/- 5 vs 117 +/- 3 mmHg for sodium-depleted and control rats, respectively).

Animals↗
PubMed1981

Depressant action of chlordiazepoxide on cardiovascular and respiratory changes induced by aversive electrical stimulation of the brain.

1. Electrical stimulation of the dorsal periaqueductal gray matter (DPAG), an aversive area of the rat brain, increased the mean blood pressure of awake rats as well as of animals anesthetized with urethane. 2. In the anesthetized rats, increases in heart rate and in breath rate were also induced by DPAG stimulation. 3. Chlordiazepoxide, a benzodiazepine, decreased the blood pressure rise caused by aversive stimulation of the brain in the awake rat. 4. Chlordiazepoxide elicited the same effect in urethane-anesthetized rats. In addition, the hyperpnea induced by electrical stimulation of the dorsal periaqueductal gray matter was also decreased by the drug. 5. The pressor response to intravenous noradrenaline was not affected by chlordiazepoxide. 6. These results suggest that benzodiazepines attenuate the neurovegetative changes accompanying emotion by depressing brain systems that integrate emotional behavior.

Animals↗
PubMed1977

Role of the baroreceptor reflex in the early phases after removing the renal artery constriction in conscious renal hypertensive rats.

Hemodynamic studies in unanesthetized rats with chronic one-kidney-Goldblatt hypertension showed a 25% increase in cardiac output and a 42% increase in peripheral resistance. Removal of renal artery constriction under either anesthesia and minor surgical trauma produced an immediate 20% drop in arterial pressure. At the end of the 6 observation period the pressure dropped 30% but still remained at a moderate hypertensive level. The hemodynamic measurement at that time suggested that the pressure drop was the result of a decrease in cardiac output. However, the data obtained 1 hour after removal of the constriction suggested that a vasodilating mechanism may also contribute to pressure normalization in the early phase of reversal of renal hypertension. In the sham-operated hypertensive rats the pressure remained unchanged, while the cardiac output dropped due to compensation by a proportional increase in peripheral resistance. In contrast, in the unclipped animals the same drop in cardiac output produced an equivalent fall in pressure because no change in peripheral resistance occurred. This was not due to an insufficiency of the baroreceptor reflex since bilateral splanchnicectomy performed at that time produced a striking hypotensive response, indicating an overactivity of the sympathetic system possibly due to the baroreceptor still reset to operate at a hypertensive level.

Animals↗
PubMed1976

Resetting of the baroreceptor in hypotension in rats.

1. A progressive but incomplete adaptation of the aortic baroreceptor was observed after 1 and 6 h of hypotension in rats subjected to controlled bleeding. Administration of phenoxybenzamine produced a greater downward displacement of baroreceptor activation range. 2. Complete adaptation was observed after 48 h of maintained hypotension in rats treated with reserpine. 3. The range of the aortic baroreceptor activation shifted upward as pressure returned to normotension, indicating the reversibility of baroreceptor adaptation in hypotension.

Adaptation, Physiological↗
PubMedDate not supplied

Tachycardic responses during the development of renal hypertension.

Basal heart rate (HR) of conscious rats under resting conditions was measured daily by electrocardiogram (ECG) during the development of one-kidney, one clip (1K1C) hypertension. A progressive increase in HR (mean +/- SEM) was observed from Day 1 to 7: 318 +/- 11; 330 +/- 18, 338 +/- 18; 344 +/- 19; 372 +/- 14; 374 +/- 11, and 388 +/- 12 bpm, respectively. During the same period, mean arterial pressure (MAP) also increase progressively: 126 +/- 2; 129 +/- 2; 134 +/- 4; 135 +/- 7; 144 +/- 2 and 157 +/- 4 mm Hg, respectively. From Day 7 onward, the HR declined, reaching values of 336 +/- 13 bpm on Day 9, with no further alterations for the next 21 days. The MAP continued to rise, however, being 158 +/- 4 on Day 8 and 175 +/- 7 mm Hg on Day 30. Sham-operated rats showed no changes in HR or MAP. During the development of hypertension, blockade of converting enzyme with captopril (10 mg/kg, i.v.) caused a significant blood pressure fall on Day 1 (-27 +/- 1 mm Hg) and Day 3 (-18 +/- 2 mm Hg), whereas on Day 6 (-9 +/- 3 mm Hg) and Day 14 (-8 +/- 3 mm Hg) the fall was not different from that of the normotensive control rats (NCR) (-6 +/- 1 mm Hg). Reflex bradycardia, produced by increasing doses of phenylephrine which elevated the MAP by 10 to 40 mm Hg, was studied in conscious NCR and renal hypertensive rats (RHR) 3 and 7 days after surgery during the development of renal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗