Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Age and elevated blood pressure are associated with blunted beta-adrenoceptor-mediated cardiovascular effects. To investigate a possible relationship between beta-adrenoceptor cardiovascular function and receptor density, beta-adrenoceptor binding capacity in mononuclear leucocytes and cardiac isoproterenol sensitivity were compared in 12 essential hypertensive and 17 normotensive subjects of comparable age. The bolus dose of isoproterenol which increased heart rate by 25 beats/min (CD25) as well as plasma norepinephrine, epinephrine, and renin activity were measured. In a radioreceptor assay using [3H]dihydroalprenolol, the antagonist binding capacity (Bmax) and the affinity constant (KD) of mononuclear leucocytes were determined. Bmax in patients was higher than in normotensive subjects (66.8 +/- 4.1 versus 48.0 +/- 3.8 SEM fmol/mg, p less than 0.05), and KD was identical in both groups. In hypertensive patients, Bmax correlated positively with age (r = 0.639, p less than 0.05) and CD25 (r = 0.593, p less than 0.05) and negatively with plasma renin activity (r = 0.679, p less than 0.05), while in normotensive subjects, Bmax correlated with CD25 only (r = 0.615, p less than 0.05). Thus, in patients with essential hypertension, a decrease in cardiac isoproterenol sensitivity and plasma renin activity is associated with an age-related increase in antagonist binding capacity. This suggests a defect in the membrane coupling of the beta-adrenoceptor effector system distal to the receptor recognition site in patients with essential hypertension.
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PMID:Increased beta-adrenoceptor binding capacity is associated with blunted beta-adrenoceptor-mediated cardiovascular responses in essential hypertension. 241 82

To investigate the impairment of beta-adrenoceptor responsiveness in human hypertension, we evaluated the effect of an oral salt load (400 mEq/day of NaCl for 7 days) on plasma catecholamine concentrations and beta-adrenoceptor-mediated effects in 11 young patients with mild essential hypertension. Responses of heart rate and plasma cAMP to isoproterenol administration were used as indices of beta-adrenoceptor responsiveness. Salt loading induced a significant reduction in the dose of isoproterenol required to raise the heart rate by 25 bpm (CD25) (from 7.6 +/- 1.5 to 5.3 +/- 0.9 micrograms, p less than 0.05) and an increase in the slopes of the regression lines for heart rate changes and isoproterenol doses (delta HR/IS) (from 3.3 +/- 0.6 to 4.7 +/- 0.7, p less than 0.05) and for plasma cyclic AMP (cAMP) level changes and isoproterenol doses (delta cAMP/IS) (from 0.3 +/- 0.06 to 1.4 +/- 0.3, p less than 0.05). After salt loading there was a significant reduction in plasma catecholamine concentrations with a significant relationship between changes in upright plasma epinephrine levels and changes in CD25 (r = 0.904, p less than 0.01) and in the slopes for delta HR/IS (r = 0.983, p less than 0.001) and delta cAMP/IS (r = 0.922, p less than 0.001). These results support the hypothesis that the impairment of beta-adrenoceptor sensitivity observed in human hypertension is associated with a beta-adrenoceptor overstimulation due to chronically elevated adrenergic tone.
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PMID:Studies of the mechanisms underlying impairment of beta-adrenoceptor-mediated effects in human hypertension. 630 32