Changes in plasma renin activity and haemodynamics during vasodilator therapy in conscious dogs with myocardial infarction or chronic volume overload

Abstract

The aim of the study was to compare the changes in plasma renin activity induced by a vasodilator in normal dogs and in dogs with an impaired cardiac reserve. In normal conscious dogs, a 60-min nitroprusside infusion increased plasma renin activity from 1.05 +/- 0.26 to 8.35 +/- 1.20 ng, angiotensin I ml-1 h-1 (P less than 0.002) and heart rate from 83 +/- 6 to 149 +/- 15 beats/min (P less than 0.002). In five dogs in which a aortocaval fistula had been created 4 weeks earlier, the same infusion still increased plasma renin activity but significantly less than in normal dogs (0.90 +/- 0.29 to 4.44 +/- 0.64 ng ml-1 h-1; P less than 0.01) and the heart rate was unchanged (134 +/- 4 to 139 +/- 7 beats/min; NS). Similarly, in five dogs with a previous myocardial infarction, the heart rats response to nitroprusside was blunted (108 to 107 beats/min;NS) and plasma renin activity increased less than in normal dogs. Plasma renin activity also increased acutely after hydralazine administration in dogs which myocardial infarction (1.05 +/- 0.26 to 8.99 +/- 0.79 ng ml-1 h-1; P less than 0.05); after 1 week of hydralazine, plasma volume had increased from 54.9 +/- 0.9 ml kg-1 to 74.5 +/- 4.9 ml kg-1 (P less than 0.05) and plasma renin activity remained higher than control (4.66 +/- 0.66 ng ml-1 h-1; P less than 0.01). In conclusion, vasodilator therapy rapidly activates vasoconstrictor forces and fluid retention even in dogs with limited cardiac reserve. Although the regulation of plasma renin secretion appears altered in these models of heart disease, the renin response remains sufficient to seriously limit the beneficial effects of vasodilator therapy.

Management of Chronic Congestive Heart Failure Caused by Myxomatous Mitral Valve Disease in Dogs: A Narrative Review from 1970 to 2020

“…During the 1980s, canine experimental studies increased compared to the 1970s [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 ], and they were mostly published in human medicine journals (DMH); in this decade, this type of study was still the most common ( Figure 3 ). However, an experimental study carried out on dogs, that was then published in a veterinary medicine journal (DMD), was identified [ 60 ].…”

Enalapril in heart failure.

“…The majority of drugs used to treat this condition, including diuretics and most vasodilators, stimulate renin release further (Nicholls et al, 1974(Nicholls et al, , 1976Markham et al, 1983;Pouleur et al, 1983). High circulating levels of angiotensin II are likely to place an added burden on the failing heart by means of a direct constrictor action on arterioles (and perhaps veins), and indirectly through stimulation of aldosterone secretion.…”

“…Activation of the renin-angiotensin system is evident during the evolution of heart failure in experimental animals (Watkins et al, 1976;Riegger et al, 1982) and in some patients with untreated cardiac failure (Brown et al, 1970;Nicholls et al, 1974). The majority of drugs used to treat this condition, including diuretics and most vasodilators, stimulate renin release further (Nicholls et al, 1974(Nicholls et al, , 1976Markham et al, 1983;Pouleur et al, 1983). High circulating levels of angiotensin II are likely to place an added burden on the failing heart by means of a direct constrictor action on arterioles (and perhaps veins), and indirectly through stimulation of aldosterone secretion.…”