In 41 normotensive volunteers (diastolic pressure, less than 90 mm Hg) the beta 2-adrenoceptor density in lymphocytes was determined by (+/-)-125 iodocyanopindolol (ICYP) binding and compared with that in nine patients with borderline hypertension (diastolic pressure, 90-95 mm Hg) and 45 patients with established essential hypertension (diastolic pressure, greater than 95 mm Hg). The mean number of beta 2-adrenoceptors for controls was 774 +/- 49 (range, 300-1,500) ICYP binding sites/cell. In borderline hypertension it was significantly higher, with 1,037 +/- 22 (range, 950-1,150) sites/cell, and increased further in patients with essential hypertension to 1,424 +/- 72 (range, 700-2,700) sites/cell. The KD values for ICYP, however, were nearly the same in all groups (approximately 50 pM). Calculation of the data of all 95 subjects resulted in a significant positive correlation between beta 2-adrenoceptor density and mean arterial blood pressure (r = 0.637; p less than 0.001). Since the properties of beta 2-adrenoceptors in human lymphocytes resemble those in other tissues, the hypothesis is presented that the increased density of beta 2-adrenoceptors may reflect sympathetic hyperactivity in essential hypertension, which might contribute (perhaps via enhanced release of endogenous noradrenaline through stimulation of presynaptic beta 2-adrenoceptors by adrenaline) to the elevation of blood pressure.

Adult↗

PubMedDate not supplied

Regression of retinal vascular changes by antihypertensive therapy.

The features of hypertensive retinal arterial vessel changes and their sequelae are reviewed. General or focal narrowing, increased reflexes or abnormal arteriovenous crossings, are often associated with, but not specific for, hypertension. They persist, with very rare exceptions, even after long-term successful antihypertensive therapy. Papilledema, cotton-wool spots, hemorrhages, and fatty exudates in malignant hypertension disappear completely within 6 to 12 months if blood pressure is well controlled. Inadequate control of elevated blood pressure delays, but does not prevent, the regression of retinopathy. The reversal into the "benign" phase may continue for years, even if blood pressure control worsens. This may be explained by a regain of autoregulation which allows the arteriolonecrotic lesions to heal. According to their size, retinal arteries are representative of the target organ of hypertensive small vessel disease. They supply a tissue that is highly sensitive to ischemia. However, even long-standing nonmalignant hypertension seems not to damage retinal tissue.

Antihypertensive Agents↗