Cardiogenic hypertension in maturing dogs.

Abstract

SUMMARY The purpose of this study was to evaluate whether the heart can induce high blood pressure by maintaining an Inappropriately elevated cardiac output/body weight ratio during growth. Direct (femoral artery) mean arterial pressure (MAP), heart rate, cardiac output/body weight ratio (as denned by M-mode echocardiography), and total peripheral vascular resistance were measured and calculated every 2 months in nine conscious dogs during development from 2 to 10 months of age. In four dogs a J-shaped catheter for a trial pacing was chronically implanted at the age of 3 months, and their hearts were permanently paced at 130 beats/min until maturity. The aim of atrial pacing was to prevent the natural slowing of the heart rate and, consequently, to maintain a cardiac output/body weight ratio that was inappropriately high in relation to age during growth. Five dogs were studied as controls. No hemodynamk differences were observed until the age of 4 months. From the age of 5 to 10 months heart rate was kept at 130 beats/min by atrial padng in the atrially paced group, and the mean cardiac output/ body weight ratio did not decrease (196 ± 24 vs 191 ± 34 [SE] ml/min/kg). MAP rose from 62 ± 4 to 116 ± 8 mm Hg, and total peripheral resistance increased from 0.34 ± 0.07 to to 0.61 ± 0.09 mm Hg/ml/min/ kg. In the control group heart rate decreased with age from 170 ± 8 to 76 ± 6 beats/min, the cardiac output/body weight ratio was reduced from 195 ± 18 to 118 ± 22 ml/min/kg, MAP increased from 65 ± 6 to 92 ± 8 mm Hg, and total peripheral resistance rose from 0.32 ± 0.09 to 0.77 ± 0.08 mm Hg/ml/min/ kg. In summary, Inappropriate elevation of the cardiac output/body weight ratio during growth caused a deviation toward higher levels of the blood pressure maturation curve and inhibited the natural rise in total peripheral resistance. We conclude that the heart may generate high blood pressure during development, but this pure cardiogenic hypertension does not trigger a secondary rise in total peripheral resistance. (Hypertension 12: 295-300, 1988) KEY WORDS • development • cardiac output • cardiogenic hypertension • atrial pacing T HE concept of cardiogenic hypertension is based on the simple hypothesis that, since arterial blood pressure is determined by both cardiac output (CO) and total peripheral resistance (TPR), the heart may play an active role in the development of some types of hypertension. '-3 Theoretical objections to such a mechanism are based on the facts that under normal conditions CO is controlled primarily by peripheral factors and the heart itself has little to do with CO regulation and that the role of the kidney in controlling blood pressure appears critical. 4 Indeed, studies in both animals and humans have shown a wide spectrum of hemodynamic variations ranging from increased TPR with a normal or low CO, to increased CO with normal TPR, to a transitional pattern with a later progressive rise in TPR. 5Nonetheless, the finding of a rise in CO of about 15% in borderline hypertension revived interest in t...

Differential gene expression and regulation of angiotensin II receptor subtypes in rat cardiac fibroblasts and cardiomyocytes in culture.

“…Subnanomolar concentrations ofAngIl facilitates adrenergic neurotransmission in the heart ( 15), indirectly leading to an increase in the heart rate, contractility, and a decrease in coronary flow ( 15,16). The majority ofthe cardiovascular and hormone modulating actions ofAng1I in the adult animal are mediated through the ATI-R (2).…”