Effects of Fosinopril on chronic nephropathy, hypertension, lipid metabolism disorders and its mechanism of action: In patients with hypertensive nephropathy treated chronically with Fosinopril at doses of 10-20 mg for 10-20 months, arterial blood pressure (systolic, diastolic, mean arterial pressure) significantly decreased, with an overall efficiency rate of 68.75%. Fosinopril demonstrates good and precise antihypertensive effects on chronic nephropathy-related hypertension. The results show that taking Fosinopril at 10-20 mg/day can significantly reduce plasma total cholesterol, triglyceride, low-density lipoprotein cholesterol, and lipoprotein (a) levels in chronic kidney disease patients while increasing high-density lipoprotein cholesterol levels, thereby improving existing lipid metabolic disorders. This finding is consistent with previous literature reports.
Kaplan's summary regarding the effects of antihypertensive drugs on lipid metabolism indicates that angiotensin-converting enzyme inhibitors have a unique effect of improving lipid metabolism through turbulence. Since 1988, when Itaven proposed the insulin resistance syndrome, it has been confirmed that insulin resistance and hyperinsulinemia play important roles in the development of hypertension and lipid metabolic disorders, acting as independent risk factors. Insulin resistance and hyperinsulinemia contribute to hypertension by promoting renal sodium reabsorption, exciting the sympathetic nervous system, increasing plasma catecholamine levels, inhibiting cell membrane Na-K-ATPase and Ca-Mg-ATPase activity, elevating intracellular calcium levels, and promoting endothelial angiotensin and endothelin-1 secretion. They also induce triglyceride synthesis and disrupt very low-density lipoprotein and low-density lipoprotein degradation, leading to reduced high-density lipoprotein synthesis and levels, thus causing lipid metabolic disorders. Therefore, improving insulin resistance and hyperinsulinemia is an effective measure for controlling hypertension and improving lipid metabolic disorders, as reported in the literature.
Angiotensin-converting enzyme inhibitors significantly improve primary hypertension, obesity-related insulin resistance, and hyperinsulinemia turbulence. Our study also proved that the angiotensin-converting enzyme inhibitor Benazepril can improve pancreatic islet function in chronic renal failure patients. Recent data shows that in chronic kidney disease patients with normal renal function, angiotensin-converting enzyme inhibitors can improve pancreatic islet dysfunction caused by insulin resistance and hyperinsulinemia. However, this paper does not report on the specific effects of angiotensin-converting enzyme inhibitors on islet turbulence. The results showed that after treatment with Fosinopril for 10-20 months at doses of 10-20 mg, the islet turbulence level and insulin area under the curve significantly dropped 30, 60, and 120 minutes after glucose load, suggesting that Fosinopril can improve existing insulin resistance and hyperinsulinemia in chronic kidney disease patients, thereby improving hypertension and lipid metabolic disorders.
The mechanisms by which angiotensin-converting enzyme inhibitors improve islet function and high turbulence resistance are not fully understood but may be associated with the inhibition of angiotensin II generation, peripheral vasodilation, increased peripheral tissue blood flow and glucose utilization, promotion of glucose transporter GLUT4 expression and activation, and promotion of peptide bradykinin and prostaglandin synthesis and transmission.