An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.

SUMMARY The interrelationship of blood pressure, cardiac output, and peripheral resistance was studied in Dahl "S" and "R" rats after 3 days on a high (8%) NaCl diet. Both "S" and "R" rats were nonnotensive when fed a normal (0.3%) NaCl diet. After 3 days of the high NaCl diet, the "R" rats remained normotensiTe (BP 112 mm Hg), while the "S" rats had an elevation of arterial pressure (BP 133 mm Hg) (p < 0.001). The cardiac outputs of both "S" and "R" rats were similar on the low NaCl diet. After 3 days of high NaCl feeding, the cardiac output of the "R" rats rose 18% above the "R" control level (p < 0.0001), while the peripheral resistance declined 14% below the "R" control level (p < 0.005), and the blood pressure (BP) did not change, a pattern quite contrary to the concept of "whole-body" autoregulation. With a similar 3-day high NaCl feeding in "S" rats, cardiac output (p < 0.005) and peripheral resistance (p < 0.05) both increased 10%, while BP rose 20%. After 7 days of high NaCl feeding, the cardiac output of the "S" rats had returned to normal, while blood pressure and peripheral resistance both continued to be elevated. This pattern of response in "S" rats could be compatible with the concept of "whole-body" autoregulation. However, since both NaCl hypertension and Goldblatt hypertension can occur in settings in which "whole-body" autoregulation appears not be to causally related, one cannot be certain whether "whole-body" autoregulation is playing a causal role in the mechanism of NaCl-induced hypertension in "S" rats. It is a striking dichotomy that 3 days of high salt feeding produces vasoconstriction in "S" rats and vasodilation in "R" rats. (Hypertension 1: 3-7, 1979) KEY WORDS • cardiac output • salt hypertension • blood pressure • diet peripheral resistance • "whole-body" autoregulation

Two lines of evidence strongly support the hypothesis that high potassium diets protect arterial endothelial cells from hypertensive damage. Stroke-prone spontaneously hypertensive rats (SHRSP) fed normal (0.75%) K or high (2.1%) K and normotensive Wistar-Kyoto rats (WKY) were examined in an endothelial function study and a histological study. In the endothelial function study, aortic rings were suspended in tissue baths to monitor isometric tension. Rings contracted with norepinephrine were tested with acetylcholine and sodium nitroprusside. In normal K SHRSP (blood pressure, 156 mm Hg), endothelium-dependent acetylcholine relaxation was severely depressed by 49% (p less than 0.001), whereas in high K SHRSP (blood pressure, 155 mm Hg), normal values were preserved. Endothelium-independent nitroprusside relaxation was virtually the same in both the SHRSP groups (high K vs normal K diet). Since indomethacin did not improve the impaired acetylcholine relaxation in normal K SHRSP, the cyclooxygenase products do not appear to have affected the endothelium-dependent relaxation in the normal K SHRSP. Thus, the endothelium-dependent relaxation response was much decreased in the normal K SHRSP and was preserved in the high K SHRSP. Thus, a high K diet appears to protect the aortic endothelium from a hypertension-induced dysfunction. In the histological study, aortic and mesenteric intimal lesions were assessed blindly under the microscope and graded from 0 to 60 for aortic and from 0 to 40 for mesenteric lesions. Aortic intimal lesion scores were 28 in normal K SHRSP (blood pressure, 209 mm Hg) and 13 in high K SHRSP (blood pressure, 207 mm Hg; -54%; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

SUMMARY Abnormally low plasma flow to renal papilla characterizes Dahl hypertension. When eating a normal Na diet (0.3% NaCl) both hypertension-seiisitive (S) rats and hypertension-resistant (R) rats, 16 weeks old, have fairly normal blood pressure (BP), averaging 144 and 129 mm Hg, respectively. However, even in this barely hypertensive state, 18 S rats bad a 31% lower papillary plasma flow (LilienTield method) than 22 R rats, 19.2 ml/100 g of papilla per min compared to 25.6 [P < 0.001). When a high (8%) NaCl diet was fed for 7 days, R rats increased papillary plasma flow from 25.6 on 0.3% NaCl to 33.8 on 8% NaCl, a 32% rise (P < 0.001). S rats increased papillary flow from 20.4 to 24.8, a 22% rise (P < 0.05). When a high (8%) NaCl diet was fed for 4 weeks, R rats increased papillary plasma flow from 25.7 ml/100 g per min on 0.3% NaCl to 29.5 ml/100 g per min on 8% NaCl, a 15% rise (P < 0.025).S rats increased papillary flow from 17.7 to 20.0 ml/100 g per min (not significant). S rats on 8% NaCl had a papillary flow 32% lower than R rats on 8% NaCl (P < 0.001). BP of S rats rose to 162 mm Hg after 4 weeks on 8% NaCl; in R rats, BP did not rise at all. S rats on 0.3% NaCl hare a low papillary flow even in a borderline hypertensive slate. When challenged with 8% NaCl, R rats increased papillary flow, an adaptation possibly important for the natriuresis. S rats failed to achieve this same high papillary flow. Lacking this adaptation, hypertension may then conceivably occur in S rats to accomplish natriuresis through a "pressure natriuresis" mechanism. Papillary flow also decreased by 11% in 26 Kyoto 17-week-old spontaneously hypertensives (BP, 182 mm Hg) compared to 24 Kyoto nonnotensives (BP, 118 mm Hg), 29.5 vs. 33.2 ml/100 g per min (P < 0.001). Thus, low papillary flow exists in both hypertensions.THE RENAL MEDULLA has several possibly important connections to hypertension. For instance, the renal interstitial cells are all located in the inner medulla.1 These cells appear to be secretory in nature and are known to secrete prostaglandin E 3 .2 Moreover, when implants of these cells are placed subcutaneously in a hypertensive rat or rabbit, some humoral agent issuing from them lowers the level of arterial pressure.3 -* These interstitial cells also contain a distinctly reduced number of cytoplasmic lipid granules in five separate forms of experimental rat hypertension.16 "' These cells not only secrete prostaglandins but also appear to elaborate Muirhead's antihypertensive neutral lipid. -'Moreover, in three forms of experimental hypertension in rats the sodium concentration in the papilla was shown to be significantly lower than that in normotensive controls.1 -*• " Also, the reduction in sodium concentration in the papilla paralleled the reduction in the number of interstitial cell granules, with a fairly strong correlation.1 -s -* Moreover, prostaglandins are very powerful vasoactive agents; in the kidney, they are synthesized (90%) mainly in the renal medulla," largely by the interstitial cells and the col...

In the United States, blacks have higher rates of hypertension than whites. A possible contributing factor to this higher rate of hypertension could be dietary differences between blacks and whites relating to sodium and potassium intake, which in turn could be related to socioeconomic differences between blacks and whites. Baseline data from the Treatment of Mild Hypertension Study (TOMHS) was used to assess differences in the urinary excretion of sodium and potassium, and the Na:K ratio between black and white participants, and also to explore the relationship of socioeconomic status (SES) and urinary electrolyte excretion within each ethnic group. Participants were men and women ages 45 to 69 with stage I diastolic hypertension (DBP < or = 99 mm Hg). Level of education and annual household income were used as indicators of SES. Two overnight urine samples were collected and analyzed for Na and K at entry on 172 black and 710 white participants. Blacks had a significantly higher mean Na:K ratio than whites, 4.3 v 3.6 (P < .001). This was primarily due to higher urinary Na excretion in blacks than whites, 57.8 v 52.7 mmol/8 h (P = .05). Analysis by education and income level showed that higher levels of urinary Na and Na:K in blacks than whites was restricted to those with lower education and income levels. For higher education and income levels, blacks had slightly lower levels of urinary Na and Na:K than whites. Correspondingly, education and income levels were related to urinary Na and Na:K in blacks but not in whites. This suggests that lower SES blacks could benefit from interventions to reduce dietary Na and increase dietary K, which would decrease their urinary Na:K ratio and may make them less prone to developing hypertension.