Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract-Obesity has been shown to be an independent risk factor for coronary heart disease. The insulin resistance associated with obesity contributes to the development of other cardiovascular risk factors, including dyslipidemia, hypertension, and type 2 diabetes. The coexistence of hypertension and diabetes increases the risk for macrovascular and microvascular complications, thus predisposing patients to cardiac death, congestive heart failure, coronary heart disease, cerebral and peripheral vascular diseases, nephropathy, and retinopathy. Body weight reduction increases insulin sensitivity and improves both blood glucose and blood pressure control. Metformin therapy also improves insulin sensitivity and has been associated with decreases in cardiovascular events in obese diabetic patients. Antihypertensive treatment in diabetics decreases cardiovascular mortality and slows the decline in glomerular function. However, pharmacological treatment should take into account the effects of the antihypertensive agents on insulin sensitivity and lipid profile. Diuretics and ␤-blockers are reported to reduce insulin sensitivity and increase triglyceride levels, whereas calcium channel blockers are metabolically neutral and ACE inhibitors increase insulin sensitivity. For the high-risk hypertensive diabetic patients, ACE inhibition has proven to confer additional renal and vascular protection. Because hypertension and glycemic control are very important determinants of cardiovascular outcome in obese diabetic hypertensive patients, weight reduction, physical exercise, and a combination of antihypertensive and insulin sensitizers agents are strongly recommended to achieve target blood pressure and glucose levels.

Our study is in agreement with previous works and shows that patients with ESRD have a higher SA index compared to those with normal renal function. In spite of having higher levels of BP no other parameter was different among apneic and nonapneic patients. Hypertension may play a pivotal role linking SA and CVD.

Arq Bras Endocrinol Metab vol 49 nº 2 Abril 2005 196 RESUMOA maior parte da adversidade atribuída à obesidade é dada pelo risco cardiovascular/coronariano imputado à mesma, particularmente presente nos obesos com distribuição visceral de gordura corporal. O acúmulo de gordura visceral está sabidamente associado à maior prevalência de desarranjos metabólicos, hormonais, inflamatórios e hemodinâmicos, que no conjunto implicarão em maior acometimento da microvasculatura e impacto negativo sobre os órgãos-alvo, particularmente sobre o eixo cárdio-renal. Neste sentido, além da associação clássica com a doença coronariana, têm-se verificado uma associação maior da obesidade visceral com a hipertrofia ventricular esquerda e microalbuminúria, ambos fatores de risco cardiovascular e nefrológico reconhecidos. Assim, a abordagem terapêutica dos pacientes obesos, particularmente dos hipertensos, deve levar em conta a estratificação de risco baseada na distribuição de gordura corporal, o que permitirá uma terapêutica mais adequada, visando-se não só o controle dos fatores de risco como a monitorização do acometimento de órgãos-alvo nestas populações. Great part of obesity adversity is due to its cardiovascular/coronary risk, particularly present in obese with visceral adiposity distribution. Visceral fat deposition is known to be associated with a greater prevalence of metabolic, neurohormonal, inflammatory and hemodynamic disorders, which together will be implicated in microvascular and target organ involvement, particularly to the cardio-renal axis. In this aspect, beyond its classical association with coronary disease, visceral obesity has been associated with left ventricular hypertrophy and microalbuminuria, which are known cardiac and nephrologic risk factors. So, therapeutic tools for obese patients, specially for those with hypertension, must accomplish the risk stratification based on body fat distribution, which will allow a more adequate therapy in terms of risk factors control as well as target organ damage monitoring. AOBESIDADE É ATUALMENTE UMA DOENÇA altamente prevalente e de elevada morbimortalidade para as populações industrializadas (1). Tal risco é particularmente atribuído às implicações cardiovasculares relacionadas à obesidade (2,3), especialmente presentes nos obesos com deposição visceral de gordura, conforme demonstrou-se nos estudos