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Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension
Insights
Essential hypertension (EH) has two forms: hyperadrenergic and hypoadrenergic. These differ in beta-adrenergic responsiveness, impacting sympathetic and renin activity, not solely explained by catecholamines.
Area of Science:
- Cardiology
- Nephrology
- Endocrinology
Background:
- Essential hypertension (EH) presents diverse pathophysiological profiles.
- Two distinct forms of EH are proposed: borderline hyperadrenergic and stable hypoadrenergic.
- These forms exhibit contrasting sympathetic and renin activity patterns.
Purpose of the Study:
- To differentiate subtypes of essential hypertension based on adrenergic and renin activity.
- To investigate the role of beta-adrenergic responsiveness in EH pathogenesis.
- To explore the kidney's involvement in adrenergic abnormalities in EH.
Main Methods:
- Assessing sympathetic and renin activity.
- Monitoring beta-adrenergic responsiveness via plasma cyclic AMP levels.
- Evaluating responses to isoproterenol and insulin-induced hypoglycemia.
Main Results:
- Borderline hyperadrenergic EH showed hyperresponsiveness of cyclic AMP, renin, and circulation to isoproterenol.
- Stable hypoadrenergic EH exhibited hyporesponsiveness of cyclic AMP and renin to insulin-induced hypoglycemia.
- The kidney plays a central role, with borderline EH showing excess urinary catecholamines.
Conclusions:
- Essential hypertension can be classified into distinct subtypes based on adrenergic and renin profiles.
- Beta-adrenergic responsiveness is a key differentiator between EH subtypes.
- Catecholamine levels alone do not fully explain the observed differences in EH forms.
Abstract:
Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.