nsulin cũng được phát hiện không cho sức mạnh huyết áp hay các hiệu ứng thận của các chất khác vasoactive, chẳng hạn như norepinephrine hoặc angiotensin-II (). Hơn nữa, trong các đối tượng béo phì, người có khả năng kháng các hiệu ứng trao đổi chất | 52 Cefalu Insulin has also been found not to potentiate the blood pressure or kidney effects of other vasoactive substances such as norepinephrine or angiotensin-II 102 103 . Further in obese subjects who are resistant to the metabolic and vasodilator effects of insulin elevated insulin did not appear to increase arterial pressure 104 . Therefore the results of several clinical research studies strongly suggest that hyperinsulinemia does not explain the increased renal tubular NaCl reabsorption shifts of pressure natriuesis or the hypertension associated with obesity in both animals and humans 101 . In contrast to the above results from rodent studies suggest that long-term elevated insulin levels may result in significant elevations in arterial pressure. This effect may be mediated through interactions with the RAS and thromboxane 101 . Studies have suggested that inhibition of thromboxane synthesis or ACE inhibition did indeed abolish the insulin-induced rise in arterial pressure in rodents 105 106 . Further blockade of endothelial-derived NO synthesis appears to enhance insulin-induced hypertension in rodents 107 . It is unclear whether these findings in rodents are relevant to the hypertension noted in obese humans but summation of the currently available studies does suggest that chronic elevated insulin levels cannot account for obesity-induced increases in blood pressure. Therefore the very close correlation between hyperinsulinemia and hypertension in obese subjects may be because obesity itself not only elevates arterial pressure but also induces peripheral insulin resistance in hyperinsulinemia through parallel but independent mechanisms 101 . The question that remains therefore is the mechanism by which obesity contributes to hypertension. A recent review by Hall et al. 101 outlines a summary of mechanisms by which obesity may cause hypertension and glomerulosclerosis by activation of the renin-angiotensin and sympathetic nervous systems including .
