Enhanced Salt Toxicity in the Spontaneously Hypertensive Rat

Abstract

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...

Effect of salt on the vascular lesions of spontaneously hypertensive rats.

“…9 Therefore, this experimental model provides the opportunity to study vascular pathology prior to acceleration of BP in response to salt-loading. The results of the present study strongly suggest that, in the SHR, salt excess induces vascular changes that are not secondary to accelerated BP increase.…”

Hypertension: A controllable disease

“…Our first experiment was with an excess of salt. 1 The drinking water was replaced with one per cent salt solution. Excess salt administration was begun when the rats were 3 months old and continued for a period of 5 months.…”

Effects of High Salt Intake on Control of Hindlimb Vascular Resistance by Arterial Broreflex and Vagal Afferents in Spontaneously Hypertensive Rats

“…A number of studies have shown that high salt intake accelerates the development of hypertension in spontaneously hypertensive rats (SHR; Barsantai et al 1971;Lois et al 1971;Aoki et al 1972). The mechanism by which high salt intake increases the severity of hypertension in SHR is not clearly defined, but several studies have indicated that the salt-induced increase in blood pressure is accompanied by an increase in sympathetic outflow (Dietz et al 1980;Winternitz & Oparill982;Chen et al 1988).…”