Differences in the regulation of vascular resistance in guinea pigs with right and left heart failure.

Abstract

SUMMARY We investigated neurogenic, non-neurogenic, and structural contributions to vascular resistance in hindquarters in five groups of guinea pigs after heart failure produced by (1) constriction of the pulmonary artery (RHF), (2) constriction of the ascending aorta (LHF A ), and (3) constriction of the descending thoracic aorta (LHF D ); (4) after left ventricular hypertrophy produced by mild constriction of the ascending aorta (LVH); and (5) after sham surgery. Pressure-flow curves were used to assess vascular resistance in the isolated, perfused hindquarters. In RHF and LHF A , vascular resistance tended to increase and for different reasons. In the LHF A group, sympathectomy produced the greatest vasodilation. Therefore, neurogenic influences predominated. The high neurogenic tone may have been related to reduced arterial pulse pressure (P < 0.05) and reflexes arising in arterial baroreceptors. In contrast, the LHF D group had increased arterial pressure and pulse pressure (P < 0.05) and normal neurogenic vasoconstriction. However, non-neurogenic vasoconstriction was increased probably as a result of increased vascular responsiveness to constrictor stimuli. In the RHF group, papaverine produced the greatest vasodilation (P < 0.05). Therefore, non-neurogenic influences predominated. This was attributed to both increased vascular responsiveness and to altered humoral stimuli. Similar maximal vasodilation indicated that structural factors contributed equally to vascular resistance in all the groups. These results indicate differences in the regulation of vascular resistance in anesthetized, guinea pig models of right and left heart failure.THE RELATIVE importance of neurogenic, humoral, vascular reactive, and structural contributions to vascular resistance in heart failure has not been established. Some investigators have suggested that the neurogenic contribution is predominant. "4 Others have reported observations that detract from this concept. In one study, for example, the reflex vasoconstrictor response to carotid occlusion was less in dogs with right heart failure than in normal dogs. 5 In two other studies reported from our own laboratory, the neurogenic influence, as estimated from the vasodilator response to sympathectomy, was not abnormally increased in hamsters with cardiomyopathy 6 or in dogs with right heart failure. 7 These observations have led us to consider the possibility that various types of heart failure might differ with regard to the relative importance of the factors regulating vascular resistance. Theoretical considerations would appear to support this possibility. Mechanoreceptors in the right and left atria may mediate different compensatory changes. Brennan et al. 8 have suggested that mechanoreceptors in the right atrium modulate plasma levels of renin. Brennan et al. 8 and Johnson et al. reflex control of vascular resistances. Thus, in left and right heart failure, which could stress different populations of mechanoreceptors, the factors contributing to vascular resistance mi...

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“…Different forms of heart failure may have one or more of the following: 1) increased neurogenic vasoconstrictor tone (i.e., neuronally released norepinephrine); 2) increased humorally delivered vasoconstrictors (e.g., norepinephrine or angiotensin); and 3) altered vascular smooth muscle reactivity (e.g., enhanced responsiveness to norepinephrine, reduced responsiveness to metabolic vasodilator stimuli). [5][6][7][8][9][10][11] Heart failure of different etiologies may use different compensatory mechanisms. For example, in animal models,5 some types of congestive heart failure (e.g., aortic stenosis with reduced stimulation of carotid arterial baroreceptors) are more likely to result in enhanced neurogenic constrictor tone than others (e.g., pulmonic stenosis, where there is an enhanced vascular constrictor response to norepinephrine).…”