Search PubMed⌕ Search

Biomedical subjects

H C Salgado

Publications and source records attributed to H C Salgado.

At least 37 records · Page 2Linked to original sources
PubMed1995

Hypertensive response to acute aortic coarctation in chronic vasopressin deficient states.

We investigated the genesis of the hypertensive response to acute (45 min) aortic constriction in two models of chronic vasopressin (AVP) deficiency, i.e., Brattleboro strain and median eminence lesioned (MEL) Wistar rats. The same degree of partial aortic constriction, with a pneumatic cuff placed around the abdominal aorta, yielded a sudden and maintained increase in carotid pressure to the same extent in Brattleboro, MEL and sham-MEL rats. Blockage of AVP V1 receptors with d(CH2)5Tyr[Me]AVP did not affect the hypertensive response of Brattleboro or MEL rats, but gradually blunted the response of sham-MEL rats. Blockage of angiotensin II receptors with saralasin blunted the hypertensive response of the AVP-deficient subjects throughout the experiment, but only delayed (5-15 min) the onset of hypertension in sham-MEL rats. Simultaneous blockage of AVP and angiotensin II blunted the hypertensive response of sham-MEL and AVP-deficient rats throughout the experiment. These data demonstrate that when one vasoactive system is chronically absent, as is the case for AVP in Brattleboro and MEL rats, the renin-angiotensin system plays the major role in the pathophysiology of acute aortic coarctation hypertension.

Angiotensin Receptor Antagonists↗
PubMed1995

Effect of chronic estradiol administration on the acute pressor response to aortic coarctation in conscious rats.

We investigated the effect of chronic estradiol administration on the pressor response elicited by acute (45 min) partial aortic constriction in conscious Wistar rats and on vascular reactivity to angiotensin II and vasopressin in vitro. Estradiol (10 micrograms kg-1 day-1, sc) or vehicle was administered for 7 days to young castrated male and female rats and to female rats that had stopped cycling (14-16 months of age). In the acute experiment of aortic coarctation in conscious rats, carotid pressure was monitored continuously before and for 45 min after partial abdominal aortic coarctation. In ovariectomized females the mean carotid pressure and heart rate before aortic coarctation were significantly lower in estradiol-treated animals (107 +/- 3 vs 119 +/- 3 mmHg and 360 +/- 31 vs 494 +/- 12 bpm). Estradiol did not affect the pressor response (145-150 mmHg) to aortic coarctation of castrated male rats or ovariectomized female rats but blunted the reflex bradycardia of ovariectomized rats. The onset of the pressor response to aortic coarctation was delayed in aged female rats as compared to the other groups. While estradiol treatment significantly accelerated the onset of hypertension in aged rats, it did not affect the pressor response of castrated animals. Full dose-response curves to angiotensin II and vasopressin were constructed in vitro in the isolated mesenteric arterial bed obtained from similarly treated groups. Estradiol did not affect the vasopressin sensitivity or responsiveness of any group, but caused a significant increase in angiotensin II sensitivity in ovariectomized rats only.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Effect of median eminence lesion on the hypertensive response due to acute aortic coarctation.

The present study was designed to investigate the effect of a lack of vasopressin resulting from electrolytic lesion of the median eminence of the hypothalamus on the acute 45-min aortic coarctation hypertension elicited in conscious rats by means of a pneumatic cuff placed around the aorta above the renal arteries. Forty-eight hours after lesion, aortic constriction elicited a prompt (5-min) rise in mean carotid pressure from 115 +/- 2 to 149 +/- 2 mmHg, followed by a gradual decline to 129 +/- 2 mmHg. In contrast, sham-lesioned rats exhibited a prompt hypertensive response from 118 +/- 2 to 157 +/- 2 mmHg that leveled off throughout the experiment. Lesioned rats treated with saralasin presented a blunted hypertensive response (within 125 +/- 2 to 130 +/- 2 mmHg), whereas sham-lesioned rats showed only a delay in the onset of hypertension. The hypertensive response of lesioned rats was unaffected by the vasopressin antagonist [d(CH2)5Tyr(Me)]AVP, whereas sham-lesioned rats submitted to this treatment presented a prompt rise in pressure followed by a gradual decline at the end of the experiment. Lesioned and sham-lesioned rats treated with saralasin plus vasopressin antagonist showed a blunted hypertensive response throughout the experiment. These data demonstrate that the integrity of the median eminence plays a pivotal role in the maintenance (30-45 min) of acute aortic coarctation hypertension, presumably involving the release of vasopressin from the neurohypophysis, whereas angiotensin II mainly accounts for the prompt (5-15 min) rise in pressure.

Acute Disease↗
PubMed1994

Blockers of the L-arginine-nitric oxide-cyclic GMP pathway facilitate baroreceptor resetting.

We investigated the role of nitric oxide on rapid (25- and 40-minute) baroreceptor resetting during the onset of acute hypertension in rats treated with NG-nitro-L-arginine, an inhibitor of nitric oxide synthesis, and methylene blue, an inhibitor of guanylate cyclase. The effect of treatment with glibenclamide, an ATP-dependent K+ channel blocker, was also investigated. Arterial hypertension was provoked in a ramp progression by the drug NG-nitro-L-arginine alone or in association with aortic coarctation. Whole aortic nerve activity and carotid pressure were recorded in the anesthetized rats. The extent of rapid resetting was evaluated by means of the ratio (delta Systolic Threshold Pressure/delta Control Diastolic Pressure) x 100 as well as by the extent of displacement of the pressure-nerve activity curve defined by the ratio (delta Mean Arterial Pressure at 50% of maximum activity/delta Mean Arterial Pressure) x 100. All groups gave the same increase in mean arterial pressure at 25 and 40 minutes after the onset of hypertension. A greater extent of resetting to hypertensive levels was observed in the treated groups compared with coarctation alone. At 40 minutes after the onset of hypertension, the coarctation and nitro-L-arginine groups exhibited a further increase in the extent of resetting. The rats submitted to glibenclamide plus coarctation presented a slight but significant decrease in gain. These findings suggest that an active L-arginine-nitric oxide-cyclic GMP pathway blunts rapid resetting during the onset of hypertension. In addition, they also indicate that ATP-dependent K+ channels can also modulate rapid resetting of the baroreceptors to hypertensive levels.

Analysis of Variance↗
PubMed1994

Chronic converting enzyme inhibition facilitates baroreceptor resetting to hypertensive levels.

We investigated the acute and chronic effects of converting enzyme inhibitors (captopril or enalapril) and of angiotensin II receptor blockade (DuP 753) on rapid (30-minute) baroreceptor resetting elicited by a prompt and sustained hypertensive response provoked by aortic constriction. Pressure-nerve activity curves, pressure at 50% of maximal baroreceptor activity, baroreceptor gain (slope of the curve), and systolic threshold pressure for baroreceptor activation were determined as indexes of baroreceptor function. A slight fall in mean arterial pressure after acute treatment with the converting enzyme inhibitor or DuP 753 was accompanied by a partial leftward curve shift, which is associated with a partial threshold shift and increase in gain. A maintained hypertensive stimulus caused a partial rightward curve shift and partial (49% to 56%) threshold shift to hypertensive levels in both acutely treated and control rats. The hypertensive stimulus provoked a partial rightward curve shift and complete (88% to 94%) threshold shift to hypertensive levels in chronically treated rats. The effect of enalapril on baroreceptor function was unaltered by the bradykinin antagonist Hoe 140. These data demonstrate that chronic inhibition of converting enzyme or blockade of angiotensin II receptors facilitates rapid resetting of the baroreceptors to hypertensive levels caused by partial aortic constriction without a change in baroreceptor sensitivity.

Angiotensin I↗
PubMed1994

Physiopathogenesis of acute aortic coarctation hypertension in conscious rats.

We investigated the role of vasopressin, angiotensin II, and catecholamines in the onset of acute (45-minute) aortic coarctation hypertension in conscious rats. Partial aortic constriction was performed by means of a pneumatic cuff placed around the abdominal aorta above the renal arteries for 15 or 45 minutes. A sham-operated group was used as control. Mean carotid pressure before aortic constriction did not differ between rat groups. Aortic constriction produced a similar increase of mean carotid pressure during 15 minutes (36 +/- 3 to 37 +/- 3 mm Hg above basal levels) and 45 minutes (37 +/- 2 to 39 +/- 3 mm Hg). Plasma vasopressin concentration after 15 minutes of coarctation (4.4 +/- 0.5 pg/mL) did not differ from that observed in control rats (3.0 +/- 0.8 pg/mL), whereas after 45 minutes, it was significantly higher (14.3 +/- 3.3 pg/mL). Plasma renin activity increased significantly after coarctation (21.7 +/- 4.1 and 29.9 +/- 2.9 ng angiotensin I/mL per hour, at 15 and 45 minutes, respectively) when compared with control rats (3.9 +/- 0.5 ng angiotensin I/mL per hour). After coarctation, plasma norepinephrine concentration was consistently reduced, whereas plasma epinephrine concentration did not differ from control rats. In conclusion, these data provide evidence for an effective vasopressor role for vasopressin in the genesis of acute (45-minute) aortic coarctation hypertension in conscious rats. In addition, although the results confirm that the renin-angiotensin system participates earlier in the onset of coarctation hypertension, they rule out a significant vasopressor role for catecholamines in the early development of hypertension.

Analysis of Variance↗
PubMed1993

Congenital coarctation of the lower thoracic aorta. A rare surgically correctable cause of hypertension in the young--case report.

We report a case of congenital coarctation of the lower thoracic aorta. The patient, a 15-year-old man, presenting with the signs of classical coarctation, had the diagnosis confirmed by an aortography. A good surgical result was achieved by means of resection of the internal shelf and aortoplasty using a bovine pericardium patch. One year after the operation the patient has normal blood pressure with good femoral pulses.

Aorta, Thoracic↗
PubMed1993

Effect of bilateral nephrectomy on hypertension produced by acute aortic coarctation.

1. The hemodynamic responses to acute (45 min) aortic coarctation were studied in conscious intact (N = 7) or bilaterally nephrectomized (N = 7) Wistar rats (250-320 g). The degree of constriction of the aorta was monitored by reducing aortic flow (measured with a pulsed Doppler flowmeter) to 40% of the basal level. 2. The nephrectomized rats presented a smaller (P < 0.05) increase in carotid pressure (14-17%) than the intact rats (25-36%). Although the aortic constriction reduced significantly the aortic flow to 40% of the basal level in both groups of rats, the calculated change in aortic resistance imposed by coarctation in the intact group was significantly (P < 0.05) higher (167-292%) than that observed (173-183%) in the nephrectomized group, except 5 min after coarctation. 3. The hemodynamic data obtained in the present study confirm our findings that nephrectomized rats display a blunted hypertensive response to acute aortic coarctation which is attributed mainly to the mechanical effect of constriction. In addition, the present data indicate that the release of vasopressor substances triggered by the kidneys in intact subjects are responsible for the gradual increase in aortic resistance during coarctation.

Acute Disease↗
PubMed1992

Chemical renal medullectomy and arterial pressure response to sinoaortic denervation.

We investigated in conscious Wistar-Kyoto rats the effect of chemical renal medullectomy on the responses of mean arterial pressure, arterial pressure lability, and heart rate to sinoaortic deafferentation (SAD). Chemical medullectomy was obtained by the intravenous administration of 2-bromoethylamine hydrobromide (2-BEA) 2-3 weeks before SAD or sham SAD. Chemically medullectomized rats were compared with control rats treated with saline. In control rats, the increase in mean arterial pressure elicited by SAD was not significantly greater than that produced by sham SAD. In medullectomized rats, SAD significantly increased mean arterial pressure compared with sham SAD. No direct relation was observed between the response of mean arterial pressure to SAD and the grade (1, 2, or 3) of lesion of the renal papilla. In control rats, SAD increased significantly arterial pressure lability. Chemical medullectomy did not affect basal lability or the increased lability after SAD. No direct relation was observed between increased arterial pressure lability due to SAD and the grade of lesion of the renal papilla. SAD produced a conspicuous tachycardia in control rats. Chemical medullectomy did not affect basal heart rate or the tachycardia produced by SAD. No direct relation was observed between the extent of this tachycardia and the grade of lesion of the renal papilla. These data indicate that lesions of the renal papilla lead to a significant increase in mean arterial pressure after SAD, without affecting basal pressure or heart rate. In addition, SAD per se did not increase significantly the mean arterial pressure in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Mechanical and neuro-humoral factors in acute aortic coarctation hypertension.

The hemodynamic responses and the role of renal nerves in the physiopathogenesis of acute (45 min) aortic coarctation hypertension were studied in conscious rats. The hemodynamic responses elicited by aortic constriction in intact and bilaterally nephrectomized rats were analyzed by means of miniaturized pulsed-Doppler flow probes. Anephric rats presented a smaller increase in mean carotid pressure (MCP) and calculated aortic resistance during aortic coarctation than did intact animals. Reflex bradycardia throughout the experiment did not differ significantly between the two groups. The pressor response following aortic coarctation in untreated renal-denervated rats was similar to that found in intact subjects. Renal-denervated rats previously treated with V1-vascular arginine vasopressin antagonist [d(CH2)5Tyr(Me)AVP] showed the same hypertensive response as control renal-denervated rats. Previous treatment of renal-denervated rats with saralasin (an angiotensin II antagonist) produced a significant reduction in the hypertensive response throughout the experiment when compared to untreated renal-denervated rats. Similarly, rats treated with the vasopressin antagonist plus saralasin showed a blunted hypertensive response following aortic coarctation. The results for rats previously treated with vasopressin antagonist plus saralasin did not differ from those obtained with saralasin alone. Overall, the results of aortic coarctation hypertension obtained in the present study indicate that: 1) Anephric rats showed a blunted hypertensive response due to the lack of neuro-humoral release of vasopressor substances (e.g. angiotensin II and vasopressin) triggered by the kidneys, when only the mechanical factor of constriction was present; 2) The lack of afferent feedback from the kidneys in renal-denervated rats for vasopressin release from the central nervous system allowed angiotensin II to play the major physiopathological role associated with the mechanical factor in the hypertensive response.

Animals↗
PubMed1991

Tachycardia during reversal of one-kidney, one-clip hypertension in conscious rats.

The efferent sympathetic activity of the heart was investigated during reversal of one-kidney, one-clip (1K,1C) hypertension in conscious, freely moving rats using changes in heart rate as an index. One-kidney, one-clip hypertensive rats presented marked tachycardia during the first 8 h after unclipping. Mean arterial pressure fell 28% 3 h after unclipping and 37% 8 h after unclipping. In a separate experiment, short term infusion (15 min) of sodium nitroprusside in conscious freely moving rats produced similar tachycardia in hypertensive and sham-operated rats. The present results indicate that the baroreceptor reflex of the heart was operating normally during the prompt reversal of hypertension after unclipping.

Animals↗
PubMed1991

Role of baroreceptor resetting in the tachycardia observed during the onset of one-kidney, one clip hypertension.

A previous study from our laboratory demonstrated the occurrence of transient tachycardia during the onset of one-kidney, one clip (1K1C) hypertension in conscious rats. In the present study, using electroneurographic recordings in anesthetized rats, we investigated the time course of baroreceptor resetting at the onset (3, 7, 14 and 21 days) of 1K-1C hypertension. No significant difference between the diastolic pressure and the systolic threshold pressure for baroreceptor activation was detected in normotensive control rats and hypertensive rats 3, 7, 14 and 21 days after clipping. These data indicate that the baroreceptors were completely reset to the hypertensive levels during the periods studied. The data also suggest that baroreceptor resetting may play a facilitating role in the onset of tachycardia and the development of 1K1C hypertension in the conscious animal model.

Animals↗
PubMed1990

Antihypertensive drugs distinctly modulate the rapid resetting of the baroreceptors.

We investigated the distinct ability of various antihypertensive drugs to modulate the extent (%) of rapid (15 minutes) resetting of the baroreceptors of normotensive rats to hypotensive levels. In one protocol, hemorrhage produced a complete resetting to hypotension in rats chronically treated (6 days) with captopril. Also, hemorrhage produced only partial resetting in rats acutely treated (10-15 minutes before baroreceptor recording) with captopril and in control (untreated) rats (73 +/- 7% and 49 +/- 5%, respectively). In another protocol, all vasodilators produced hypotension in normotensive rats. Nifedipine produced complete (93 +/- 4%) resetting to hypotension, whereas prazosin produced near-maximal (83 +/- 3%) resetting. The remaining drugs studied (phenoxybenzamine, trimethaphan, and MgSO4) induced a partial resetting (63 +/- 7%, 63 +/- 9%, and 50 +/- 5%, respectively) that did not differ significantly from the extent observed with hemorrhage in control (untreated) rats. These results demonstrate that different antihypertensive drugs distinctly modulate rapid baroreceptor resetting to hypotensive levels and that nifedipine and long-term treatment with captopril associated with hemorrhage modulate rapid resetting to hypotension in a more efficient manner.

Animals↗
PubMed1990

Intrinsic heart rate after infusion of angiotensin II in rats with sino-aortic deafferentation.

We investigated the effect of the infusion of angiotensin II on intrinsic heart rate in rats with sino-aortic deafferentation. Sino-aortic deafferentated (SAD) rats studied 48 h after surgery presented significant tachycardia when compared with sham-operated rats (426 +/- 16 vs 338 +/- 6 bpm), but no change in intrinsic heart rate (369 +/- 9 vs 369 +/- 11 bpm). Infusion of angiotensin II into the SAD group 48 h after deafferentation did not produce an additional increase in heart rate (423 +/- 16 vs 426 +/- 16 bpm) or a change in intrinsic heart rate (369 +/- 11 vs 369 +/- 9 bpm) when compared with sham-operated rats submitted to saline infusion. Intravenous (iv) infusion of angiotensin II into sham-operated rats produced a significant increase in both heart rate (381 +/- 12 vs 338 +/- 6 bpm) and intrinsic heart rate (427 +/- 9 vs 369 +/- 11 bpm). These data indicate that a) tachycardia after SAD is not associated with an increase in intrinsic heart rate, b) in sham-operated rats, the tachycardia occurring after angiotensin II infusion is associated with an increase in intrinsic heart rate, and c) angiotensin II infusion does not alter the intrinsic heart rate of rats tested 48 h after sino-aortic deafferentation. We conclude that the increase in intrinsic heart rate caused by angiotensin II in conscious rats depends on the integrity of the baroreceptor reflex.

Afferent Pathways↗
PubMed1990

Baroreceptor resetting facilitates the onset of one-kidney, one clip hypertension.

1. A previous study from our laboratory demonstrated the occurrence of transient tachycardia during the onset of one-kidney, one clip (1K1C) hypertension in conscious rats. In the present study, using electroneurographic recordings in anesthetized rats, we investigated the time course of baroreceptor resetting at the onset (3, 7, 14 and 21 days) of 1K1C hypertension. 2. There was no significant difference between the diastolic pressure of hypertensive animals and the systolic threshold pressure for baroreceptor activation in normotensive control rats (100 +/- 3 vs 92 +/- 5 mmHg), and hypertensive rats 3 (118 +/- 3 vs 112 +/- 5 mmHg), 7 (125 +/- 6 vs 119 +/- 5 mmHg), 14 (135 +/- 11 vs 125 +/- 10 mmHg) and 21 (154 +/- 6 vs 150 +/- 8 mmHg) days after clipping. 3. These data indicate that the baroreceptors were completely reset to the hypertensive levels during the periods studied and also suggest that baroreceptor resetting may play a facilitatory role for the onset of tachycardia and the development of 1K1C hypertension in the conscious animal model.

Analysis of Variance↗
PubMed1989

Acute aortic coarctation hypertension: role of vasopressin and angiotensin II.

The role of vasopressin (AVP) and angiotensin II (ANG II) in the onset of acute (45 min) aortic coarctation hypertension was studied in conscious rats. Changes in mean carotid pressure (MCP) and heart rate (HR) were measured in four groups of rats. Control rats presented a hypertensive response that attained a plateau 5 min after coarctation and remained near this level throughout the experiment. Rats treated with AVP V1-vascular receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5Tyr(Me)AVP] presented a prompt rise in MCP similar to the control rats, but in contrast to this group, the MCP started to decline progressively. Rats treated with saralasin presented a delay in the onset of hypertension right after coarctation but slowly attained values similar to those for control rats. In contrast, the rats treated with AVP antagonist plus saralasin showed a blunted MCP elevation throughout the experiment. Reflex bradycardia observed in the rats treated with saralasin or the AVP antagonist plus saralasin was similar to that observed in the control rats, whereas for the group treated only with AVP antagonist, the reflex bradycardia was more intense than for the other three groups, indicating an increased sensitivity of the baroreflex. These data demonstrate that in addition to the mechanical effect of aortic constriction, both ANG II and AVP participate in the onset of acute aortic coarctation hypertension. Moreover, the results indicate that ANG II acts on the prompt (5 min) rise in pressure, whereas AVP is responsible for the maintenance (30-45 min) of the arterial pressure elevation.

Acute Disease↗
PubMed1988

Tachycardia during the onset of one-kidney, one-clip renal hypertension: role of the renin-angiotensin system and AV3V tissue.

We have previously demonstrated a transitory tachycardia during the early phase of one kidney, one clip (1K1C) hypertension in the rat, when the basal heart rate (HR) is measured daily under resting conditions. In the present study, in control rats, marked tachycardia (406 +/- 11 vs 320 +/- 4 bpm during the control period) was observed on the first day of electrolytic lesion of the anteroventral third ventricle (AV3V) region. The basal HR declined progressively thereafter and was normal 14 days after AV3V lesion. The peak of tachycardia (388 +/- 12 bpm) observed 7 days after clipping in sham-lesioned rats did not occur in 1K1C AV3V-lesioned rats (318 +/- 5 bpm). However, hypertension was only partially (65%) abolished in the lesioned animals (135 +/- 4 vs 160 +/- 3 mm Hg in the sham-lesioned 1K1C). Captopril administered per os (30 mg/kg/day) for up to 20 days produced no change in the basal HR of sham-operated rats but abolished the initial tachycardia in 1K1C rats during the development of hypertension. Captopril also delayed the onset of renal hypertension, with mean arterial pressure reaching hypertensive levels only 2 weeks after clipping. These data indicate that integrity of the AV3V region is necessary for the occurrence of tachycardia during the onset of 1K1C hypertension. Since captopril abolished the tachycardia, the activity of converting enzyme seems to be important for the appearance of this phenomenon.

Animals↗