Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats

Ouabain increases vascular resistance and may induce hypertension by inhibiting the Na+ pump. The effects of 0.18 and 18 µg/kg, and 1.8 mg/kg ouabain pretreatment on the phenylephrine (PHE; 0.1, 0.25 and 0.5 µg, in bolus)-evoked pressor responses were investigated using anesthetized normotensive (control and uninephrectomized) and hypertensive (1K1C and DOCA-salt treated) rats. Treatment with 18 µg/kg ouabain increased systolic and diastolic blood pressure in all groups studied. However, the magnitude of this increase was larger for the hypertensive 1K1C and DOCA-salt rats than for normotensive animals, while the pressor effect of 0.18 µg/kg ouabain was greater only in DOCA-salt rats. A very large dose (1.8 mg/kg) produced toxic effects on the normotensive control but not on uninephrectomized or 1K1C rats. Rat tail vascular beds were perfused to analyze the effects of 10 nM ouabain on the pressor response to PHE. In all animals, 10 nM ouabain increased the PHE pressor response, but this increase was larger in hypertensive DOCA-salt rats than in normotensive and 1K1C rats. Results suggested that a) increases in diastolic blood pressure induced by 18 µg/kg ouabain were larger in hypertensive than normotensive rats; b) in DOCA-salt rats, smaller ouabain doses had a stronger effect than in other groups; c) hypertensive and uninephrectomized rats were less sensitive to toxic doses of ouabain, and d) after treatment with 10 nM ouabain isolated tail vascular beds from DOCA-salt rats were more sensitive to the pressor effect of PHE than those from normotensive and 1K1C hypertensive rats. These data suggest that very small doses of ouabain, which might produce nanomolar plasma concentrations, enhance pressor reactivity in DOCA-salt hypertensive rats, supporting the idea that endogenous ouabain may contribute to the increase and maintenance of vascular tone in hypertension.

Effects of mercury on the arterial blood pressure of anesthetized rats

The available data suggests that hypotension caused by Hg2+ administration may be produced by a reduction of cardiac contractility or by cholinergic mechanisms. The hemodynamic effects of an intravenous injection of HgCl2 (5 mg/kg) were studied in anesthetized rats (N = 12) by monitoring left and right ventricular (LV and RV) systolic and diastolic pressures for 120 min. After HgCl2 administration the LV systolic pressure decreased only after 40 min (99 ± 3.3 to 85 ± 8.8 mmHg at 80 min). However, RV systolic pressure increased, initially slowly but faster after 30 min (25 ± 1.8 to 42 ± 1.6 mmHg at 80 min). Both right and left diastolic pressures increased after HgCl2 treatment, suggesting the development of diastolic ventricular dysfunction. Since HgCl2 could be increasing pulmonary vascular resistance, isolated lungs (N = 10) were perfused for 80 min with Krebs solution (continuous flow of 10 ml/min) containing or not 5 µM HgCl2. A continuous increase in pulmonary vascular resistance was observed, suggesting the direct effect of Hg2+ on the pulmonary vessels (12 ± 0.4 to 29 ± 3.2 mmHg at 30 min). To examine the interactions of Hg2+ and changes in cholinergic activity we analyzed the effects of acetylcholine (Ach) on mean arterial blood pressure (ABP) in anesthetized rats (N = 9) before and after Hg2+ treatment (5 mg/kg). Using the same amount and route used to study the hemodynamic effects we also examined the effects of Hg2+ administration on heart and plasma cholinesterase activity (N = 10). The in vivo hypotensive response to Ach (0.035 to 10.5 µg) was reduced after Hg2+ treatment. Cholinesterase activity (µM h-1 mg protein-1) increased in heart and plasma (32 and 65%, respectively) after Hg2+ treatment. In conclusion, the reduction in ABP produced by Hg2+ is not dependent on a putative increase in cholinergic activity. HgCl2 mainly affects cardiac function. The increased pulmonary vascular resistance and cardiac failure due to diastolic dysfunction of both ventricles are factors that might contribute to the reduction of cardiac output and the fall in arterial pressure.

Resposta da pressão arterial ao esforço em adolescentes: influência do sobrepeso e obesidade

Artigo original Ergoespirometria

Monitorização ambulatorial da pressão arterial em indivíduos normotensos submetidos a duas sessões únicas de exercícios : resistido e aeróbio

Objetivo: investigar a influência de duas sessões únicas de exercício resistido (circuito com pesos) e aeróbio sobre as alterações pressóricas, em indivíduos sedentários e normotensos. Métodos: foram avaliados pela monitorização numa situação controle, sem realização de exercícios (MAPA 1) 25 indivíduos, após exercício resistido (MAPA 2) e após exercício aeróbio (MAPA 3). Os exercícios resistidos foram realizados sob forma de circuito com pesos, com intensidade de 40% da força máxima individual e os exercícios aeróbicos em cicloergômetro, com intensidade entre 60% e 70% da freqüência cardíaca (FC) máxima alcançada no teste ergométrico. Resultados: a pressão arterial sistólica (PAS) de 24h e sub-períodos vigília e sono não apresentaram variações estatisticamente significantes quando comparada à MAPA2 e MAPA3 e MAPA2 e MAPA3 entre si. A pressão arterial diastólica (PAD) de 24h e diurna apresentaram reduções significantes (P<0,05). A média da freqüência cardíaca de 24h e no período vigília apresentou aumentos significativos (P<0,05) quando comparada a MAPA2 à MAPA3. Conclusão: uma sessão única de exercício resistido em indivíduos normotensos foi suficiente para promover reduções significativas dos níveis tensionais, no período de sono após o exercício, e a de exercício aeróbio nesses mesmos indivíduos, foi mais eficaz em promover reduções significativas dos níveis pressóricos.

Oral rapamycin attenuates atherosclerosis without affecting the arterial responsiveness of resistance vessels in apolipoprotein E-deficient mice

The objective of the present study was to assess the effects of the immunosuppressant rapamycin (Rapamune®, Sirolimus) on both resistance vessel responsiveness and atherosclerosis in apolipoprotein E-deficient 8-week-old male mice fed a normal rodent diet. Norepinephrine (NE)-induced vasoconstriction, acetylcholine (ACh)- and sodium nitroprusside (SNP)-induced vasorelaxation of isolated mesenteric bed, and atherosclerotic lesions were evaluated. After 12 weeks of orally administered rapamycin (5 mg·kg-1·day-1, N = 9) and compared with untreated (control, N = 9) animals, rapamycin treatment did not modify either NE-induced vasoconstriction (maximal response: 114 ± 4 vs 124 ± 10 mmHg, respectively) or ACh- (maximal response: 51 ± 8 vs 53 ± 5%, respectively) and SNP-induced vasorelaxation (maximal response: 73 ± 6 vs 74 ± 6%, respectively) of the isolated vascular mesenteric bed. Despite increased total cholesterol in treated mice (982 ± 59 vs 722 ± 49 mg/dL, P < 0.01), lipid deposition on the aorta wall vessel was significantly less in rapamycin-treated animals (37 ± 12 vs 68 ± 8 µm2 x 103). These results indicate that orally administered rapamycin is effective in attenuating the progression of atherosclerotic plaque without affecting the responsiveness of resistance vessels, supporting the idea that this immunosuppressant agent might be of potential benefit against atherosclerosis in patients undergoing therapy.

Neural reflex regulation of arterial pressure in pathophysiological conditions : interplay among the baroreflex, the cardiopulmonary reflexes and the chemoreflex

The maintenance of arterial pressure at levels adequate to perfuse the tissues is a basic requirement for the constancy of the internal environment and survival. The objective of the present review was to provide information about the basic reflex mechanisms that are responsible for the moment-to-moment regulation of the cardiovascular system. We demonstrate that this control is largely provided by the action of arterial and non-arterial reflexes that detect and correct changes in arterial pressure (baroreflex), blood volume or chemical composition (mechano- and chemosensitive cardiopulmonary reflexes), and changes in blood-gas composition (chemoreceptor reflex). The importance of the integration of these cardiovascular reflexes is well understood and it is clear that processing mainly occurs in the nucleus tractus solitarii, although the mechanism is poorly understood. There are several indications that the interactions of baroreflex, chemoreflex and Bezold-Jarisch reflex inputs, and the central nervous system control the activity of autonomic preganglionic neurons through parallel afferent and efferent pathways to achieve cardiovascular homeostasis. It is surprising that so little appears in the literature about the integration of these neural reflexes in cardiovascular function. Thus, our purpose was to review the interplay between peripheral neural reflex mechanisms of arterial blood pressure and blood volume regulation in physiological and pathophysiological states. Special emphasis is placed on the experimental model of arterial hypertension induced by N-nitro-L-arginine methyl ester (L-NAME) in which the interplay of these three reflexes is demonstrable.

Hipertensão arterial e consumo de sal em população urbana

Objetivo: Avaliar o consumo de sal e a relação sódio/potássio urinário em amostra randomizada de população urbana etnicamente miscigenada. Métodos: Foi selecionada uma amostra randômica de 2.268 residentes de Vitória, ES, entre 25 e 64 anos de idade. Os indivíduos foram escolhidos por amostragem domiciliar realizada em 1999/2000, dos quais 1.663 (73,3%) compareceram ao hospital para a realização de exames padronizados. O consumo estimado de sal, Na+ e K+ foi determinado por meio da coleta de urina de 12h no período noturno (19h às 7h) e do gasto mensal de sal domiciliar referido durante a entrevista. A pressão arterial clínica foi medida duas vezes por diferentes pesquisadores treinados em condições padronizadas, usando esfignomamômetro de mercúrio. Para análise estatística foram utilizados o teste de Student e o teste de Tukey. Resultados: A excreção urinária de Na+ foi mais alta em homens e em indivíduos de menores condições socioeconômicas (P<0,000). Não foi observada diferença entre os grupos étnicos. A excreção de K+ não se relacionou com nível socioeconômico e raça, mas foi significativamente mais alta entre os homens (25±18 x 22±18 mEq/12h; P=0,002). Foi observada uma correlação linear positiva entre a excreção urinária de Na+ e pressão arterial sistólica (r=0,15) e diastólica (r=0,19). Indivíduos hipertensos apresentaram maior excreção urinária de Na+ e relação Na/K, quando comparados com indivíduos normotensos. O consumo de sal relatado foi aproximadamente 50% do consumo estimado pela excreção urinária de 12h (em torno de 45% da excreção urinária de 24h). Conclusões: A ingestão de sal é fortemente influenciada pelo nível socioeconômico e pode, parcialmente, explicar a alta prevalência de hipertensão arterial nas classes socioeconômicas mais baixas