Nitrendipine-based antihypertensive therapy is particularly beneficial in older patients with diabetes and isolated systolic hypertension. Thus, our findings do not support the hypothesis that the use of long-acting calcium-channel blockers may be harmful in diabetic patients.

No abstract

SUMMARY A 40-year-old man was admitted to the hospital with pulmonary edema without signs of left ventricular failure. Noncardiogenic pulmonary edema was diagnosed, and a subsequent workup identified a pheochromocytoma as the cause of this condition. The clinical picture could be mimicked by infusion of exogenous norepinephrine. It is concluded that surges of catecholamines from a pheochromocytoma may provoke pulmonary edema in a manner similar to that by which neurogenic pulmonary edema related to cerebral disorders occurs. (Hypertension 8: 810-812, 1986) KEY WORDS • catecholamines • heart failure * hypertension P RESSOR crises, excessive sweating, and headache are among the most frequent symptoms of pheochromocytoma. 1 Furthermore, pulmonary edema may develop as a result of cardiac failure. The latter usually is due to a sudden or sustained rise in arterial pressure or the result of catecholamine-induced cardiomyopathy.1 ' 2 We report on a patient with pheochromocytoma in whom several episodes of pulmonary edema occurred in the absence of hypertension and without signs of left ventricular dysfunction.Case Report A 40-year-old man was admitted to the coronary care unit because of acute, severe dyspnea and production of blood-stained sputum. He had been well until 8 years earlier when he was involved in a car accident and remained comatose for 24 hours. Since that time he had had several bouts of mild dyspnea accompanied by feelings of unease and restlessness. Although such episodes were short-lived, the patient had noticed an increased frequency over the previous 2 or 3 months.On examination he appeared tachypneic, cyanotic, and clammy. Supine blood pressure was 80/60 mm Hg, and the heart rate was 115 beats/min. The heart was normal, and no ventricular gallop was heard, but numerous rales were audible in both lungs. No other abnormalities were evident. Laboratory investigation disclosed slightly elevated hemoglobin levels (12 mmol/L), hematocrit (59%), and creatinine levels (135 /xmol/L). The levels of serum glutamic-oxalacetictransaminase, serum glutamic-pyruvate transaminase, and lactic dehydrogenase were modestly increased, but the creatinine kinase level was normal. A chest roentgenogram showed massive pulmonary edema but a normal-sized heart; an electrocardiogram revealed sinus tachycardia and signs of right ventricular strain with no evidence of myocardial infarction. After a Swan-Ganz thermodilution catheter had been introduced, the following hemodynamic data were obtained: pulmonary artery pressure, 21/3 mm Hg (mean, 12 mm Hg); pulmonary capillary wedge pressure, 2 mm Hg; right atrial pressure, 0 mm Hg. Cardiac output was 3.45 L/min, while intra-arterial pressure was still low: 75/55 mm Hg. All measurements were done while the patient was still recumbent. Calculated systemic vascular resistance was normal, but pulmonary vascular resistance was increased. Treatment consisted of oxygen by mask and infusion of plasma and the patient recovered within a few hours. Cardiac output then stabilized at 7 L/min...

Angiotensin II (Ang II) acts at the cellular level on two receptor subtypes: the AT1 receptor which can be blocked by losartan and its analogues (the 'sartan family'), and the AT2 receptor that does not react with the above antagonists but which can be blocked by different compounds, such as PD123319. AT1 receptor blockade has proven to be a highly effective means of interference with the renin-angiotensin system (RAS) and hence of reducing high blood pressure. As a result of the terminal blockade of the RAS cascade, circulating Ang II levels tend to rise two- to threefold. The free access of such enhanced levels to uninhibited AT2 receptors may be clinically relevant, as argued in the present review. The most extensive experimental and clinical experience with AT1 receptor blockade so far has been obtained with the pioneer drug losartan, although major contributions have also been made on candesartan cilexetil, irbesartan and valsartan. All of these four drugs have been instrumental in substantial clinical trials, serving as sources of information in the clinically oriented part of this review. AT1 receptor blocking drugs generally provide a relatively gradual decrease in blood pressure, which is comparable to that obtained with conventional anti-hypertensive drugs. Clinical trials reveal an astounding lack of drug-related adverse effects, scoring even better than placebo in terms of frequencies and sometimes patterns. The trough/peak ratio on single dosages seems to have been mastered, particularly with the second generation of AT1 receptor blockers, as is evident from 24 h ambulatory blood pressure monitoring. Combination with low-dose thiazide regimens is well established. Intermediate endpoints (micro-albuminuria and left ventricular hypertrophy) appear to be controllable. Morbid cardiovascular sequelae are currently under study in comparison with beta- and calcium channel blockade.

Ischaemic and degenerative brain diseases are a major health problem leading to a devastating loss of autonomy. Hypertension has been shown to carry an increased risk not only for cerebrovascular morbidity and mortality but also for cognitive impairment and dementia. Although diastolic blood pressure is considered an important risk factor, it is now clear that isolated systolic hypertension and elevated pulse pressure also play an important role in the development of brain complications. Therefore the treatment of these conditions must urgently become a widespread tool of prevention. All the randomised placebo-controlled trials completed for the last 30 years have shown a reduction in fatal and/or non-fatal strokes. In the most recent trials in isolated systolic hypertension in older patients, the benefit was even greater because of the higher risk in these populations. The new classes of drugs, in particular, calcium-channels blockers and angiotensin-