The blood pressure of spontaneously hypertensive rats was controlled at low normotensive levels, using antihypertensive drugs for a 6-month period beginning when the rats were 3 months of age. Treatment was then withdrawn and the rats observed for an additional 4 months, until they were 13 months of age. Treatment with antihypertensive drugs arrested the progression of the hypertension and the secondary pathology for the duration of the treatment period. Following withdrawal of drugs the blood pressure did not rise to the level of the controls of a similar age, but rather it returned to the level that existed before treatment began and then progressed at the same rate that the controls exhibited when they were 3-7 months of age. Pathological changes were found only in controls. These results indicate that, although the tendency toward hypertension is inherited, its rate of development depends on environmental factors. The hypei tension can be arrested by chemotherapeutic interventions and can be aggravated by excessive salt. The hypertension appears to be a progressive time-dependent process but is independent of biological processes associated with aging per se. Finally, control of blood pressure prevents end-organ damage. • The spontaneously hypertensive rat presents an experimental model which in many ways resembles essential hypertension in man (1). One of the great advantages of this model is that the entire life history of the disease is compressed within a period of less than 2 years. Clinically, in the treatment of patients with essential hypertension, it has been observed that, following prolonged reduction of blood

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In 1950, Sapirstein et al. ( 1 ) demonstrated that rats developed hypertension when given 2 % NaCl solution to drink for 6 weeks. Dahl et al. (2,3) develloped two strains of Sprague-Dawley rats, one of which became hypertensive rapidly when fed an excess salt diet while the other was resistant to salt. These two strains remained consistent as hypertension-sensitive and hypertensionresistant with other melthods of creating experimental hypertensiojn, such as clipping one renal artery (4). In 1963, Okamoto and Aoki ( 5 ) produced by selective inbreeding a spontaneously hypertensive strain of Wistar rats (SHR) whose members developed elevated blood pressures as they matured. Louis et al. (6) tested the effect of salt consumption on this SHR strain and concluded that their blood pressures were relatively mresponsive to excessive sodium intake. Such a result is at variance with the experience of Dahl and also is inconsistent with Okamoto's observations that SHR responded with a greater rise in blood pressure than control rats when given DOCA plus 1% NaCl for 10 weeks or following unilateral nephrec toniy ( 7 ) . The present study was undertaken to reexamine the question as to whether SHR developed more severe hypertension than normal (noa-SH) Wistar rats when subjected to a prolonged period of excess salt ingestion.Methods. Six male and 8 female SHR derived from the strain developed by Okamoto and Aoki were divided into two groups each consisting of 4 females and 3 lmales. The membership of the groups was determined by matching average systolic pressures and body weights. One group received 1% NaCl in tap water ad libitum while the control group was given plain tap water. All rats ate Wayne chow. They were housed in plastic cages, three males or four females to a cage. Two control groups of 3-month-old normal (non-SH) Wistar rats were also formed. Three males and three females received the 1% NaCl solution while one female and two males received tap water without excess salt.All rats were kept in a room controlled at a constant temperature of 78°F. Systolic blood pressures were recorded approximately every 2 weeks in this room by means of a tail cuff and mercury-in-rubber resistance gauge. The inflatable cuff was connected to a Statham transducer attached to a Hewlett-Packard carrier preamplifier and 2-channel recorder. The other channel of the recorder was connected through another preamplifier and a small Wheatstme bridge to the resistance gauge which detected the change in tail circumference occurring at the time of the first pulse appearing distal to the tail cuff. The rats were lightly anesthetized with ether during pressure measurements. The animals were weighed every 2 weeks.Results. Water consumptison. SH rats receiving 1% salt solution drank 2 to 3 times more than those on tap water from the third week and 1 to 3 times more than the normal rats on the same salt regimen (Table I ) . Water consumption in the SH rats receiving salt increased with time until the majority had died. Normal rats receiving excess s...

Hypercalcemia associated with head and neck malignancy is not an uncommon occurrence; its causes are multiple. Eight hypercalcemic patients with head and neck malignancy were studied. Serum calcium, serum phosphorus, tubular phosphorus threshold, fasting calcium excretion, plasma 1,25-dihydroxyvitamin D, nephrogenous cyclic adenosine monophosphate (AMP), and immunoreactive parathyroid hormone were measured. Excessive dietary calcium administration in the form of an oral hyperalimentation preparation appeared to be the cause of hypercalcemia in 2 patients. Six patients demonstrated humorally mediated hypercalcemia. These patients resembled patients with primary hyperparathyroidism in having elevated nephrogenous cyclic AMP excretion and reduced proximal tubular phosphorus reabsorption, but they differed from patients with primary hyperparathyroidism by having normal levels of immunoreactive parathyroid hormone, markedly increased fasting calcium excretion, and strikingly reduced mean plasma levels of 1,25-dihydroxyvitamin D. These data strongly suggest that the humoral factor responsible for hypercalcemia in patients with head and neck cancer is not parathyroid hormone, and that patients with hyperparathyroidism can now be distinguished with confidence from those with malignancy-associated hypercalcemia.

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