Chronic caffeine ingestion exacerbates 2-kidney, 1-clip hypertension and ameliorates deoxycorticosterone acetate-salt hypertension in rats.

The present study was aimed to determine the effect of caffeine on the development of renal hypertension. Two-kidney, 1-clip (2K1C) hypertension and deoxycorticosterone acetate (DOCA, 200 mg/kg, subcutaneous implantation)-salt (0.9% NaCl drinking) hypertension were instituted in Sprague-Dawley rats. They were then grouped into two groups each: one was supplemented with caffeine (0.1%) in their drinking solution and the other was not. Systolic blood pressure was measured up to 24 days. Caffeine exacerbated the development of 2K1C hypertension in association with a higher plasma renin concentration (PRC). Caffeine ingestion, however, did not exacerbate but ameliorated DOCA-salt hypertension in which PRC was comparable between the caffeine-ingested and control groups. Concentrations of plasma atrial natriuretic peptide (pANP) were significantly different between the caffeine-ingested and control groups neither in 2K1C nor in DOCA-salt rats, suggesting that ANP was not responsible for the modified blood pressure. Acute caffeine infusion (350 micrograms/min, 30 min) in anesthetized normotensive rats caused increases in urinary excretion (volume and sodium) and in PRC without significantly affecting the blood pressure and pANP. These results suggest that caffeine specifically exacerbates 2K1C hypertension through increasing renin release whereas it ameliorates DOCA-salt hypertension possibly through increasing renal excretion.