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6266.7 vs 266 165 pg/ml (p,0.001); adrenaline 41.83 68.44 vs 20.35 68.46 pg/ml (p50.05); PRA 0.4960.37 vs 0.3560.21ng/ml/hr (NS); aldosterone 111.7654.5 vs 56.45 624.3 pg/ml (p,0,005); cortisol 147.27 685.9 vs 90.36640.6 ng/ml (p,0.02). fT3 was inversely related to diastlolic BP, noradrenaline, adrenaline, aldosterone and cortisol (r 50.58, p,0.004; r5.56, p,0,01; r50.41, p, 0.05; r50.51, p,0.02; r50.50 p,0.02; respectively); opposite correlations were found for TSH. A sympathetic and adrenal activation was observed in hypothyroidism which paralleled the increase in arterial blood pressure and was subsequently reversed with the restoration of thyroid hormone treatment. These mechanisms can represent causal factors in the development of arterial hypertension in human hypothyroidism. Hypothyroidism should be screened in hypertensive patients. If found affected, they could beneflt from the thyroid substitutive therapy also as an antihypertensive treatment.

Elevated blood pressure in patients with hydronephrosis and unilateral renal dysfunction