Potassium infusion attenuates avoidance-saline hypertension in dogs.

Abstract

SUMMARY Previous studies have shown that a combination of avoidance conditioning schedules and increased intake of salt and water results in progressive hypertension in dogs within 14 days. The present experiments investigated the effects of increasing potassium intake upon blood pressure and heart rate of dogs made hypertensive by avoidance conditioning and salt-water loading. Two daily 30-minute sessions of free-operant avoidance conditioning were presented for 36 days during which isotonic saline was continuously infused into the arterial circulation (1.2 liters/day; 185 mEq Na + ). Daily mean levels of systolic ( to a combination of free-operant avoidance conditioning schedules and continuous infusion of isotonic saline results in progressive hypertension within 14 days, accompanied by no consistent changes in heart rate levels. '• 2 By contrast, exposure of dogs to avoidance schedules under conditions of normal sodium intake, or salt-water loading without avoidance stress, typically produces no significant blood pressure changes over the same time periods. This new model of rapidly-developing hypertension requires no specific genetic bias, surgical alteration of kidney functions, or administration of steroids.Several models of experimental hypertension have been developed previously in rodents which involve increases in salt intake but no systematic aversive stimulation. For example, significant blood pressure elevations have been observed as a function of salt feeding in rats with genetic bias, 3 ' 4 surgical alteration of renal

Behavioral stress potentiates the blood pressure effects of a high sodium intake.

“…A more extended period of high sodium intake might result in larger magnitude elevations in blood pressure, as might a higher dose of sodium chloride supplementation (20) or concurrent restriction of dietary potassium (21)(22)(23). Few subjects in this study were from special populations (e.g., blacks, elderly, hypertensives) demonstrated to have a high prevalence of sodium sensitivity (24,25).…”

Neuroendocrine profiling in inherited stress-induced arterial hypertension rat strain with stress-sensitive arterial hypertension

“…Support has come from extensive clinical practice (Kaplan 1978, Zimmerman & Frohlich 1990, Schneider et al 2005, Šantić et al 2006) and experimental research (Lawler et al 1981, Anderson et al 1983, Sanders & Lawler 1992, Henry et al 1995, Ely et al 1997, Mormede 1997, McDougall et al 2004. It is common knowledge that repeated exposure to stressful situation or the chronic stress state with elevated blood pressure may lead to persistent arterial hypertension (Kulkarni et al 1998, Kario et al 2003, Grassi & Mancia 2004.…”

High Stress Responsivity Predicts Later Blood Pressure Only in Combination With Positive Family History and High Life Stress

“…Three key examples are (1) the modified social environments that enhance confrontations regarding dominance in mice, rats, and monkeys, 19 -25 (2) the model of Received October 9, 1998; first decision December 4, 1998; revision accepted January 26, 1999 daily exposure to shock avoidance conflict in the borderline hypertensive rat (BHR), 26 -30 and (3) the model of combined daily shock avoidance plus saline infusion in the dog. [31][32][33] Each of the models demonstrates that stress exposure can be a critical factor leading directly to hypertension but also that hypertension will only occur in those animals with high susceptibility due to genetic and/or environmental factors. Recent extensions of Henry's work has shown that hypertension with his model develops in only the most susceptible rat strains, and then only in the aggressive dominant or just subdominant males.…”

“…[23][24][25] Similarly, the BHR model is highly susceptible to either salt-induced or stress-induced hypertension because of genetic influences from its 1 spontaneously hypertensive rat (SHR) parent, 30 and the dog model is susceptible because of excessive salt intake combined with potassium deficiency. 32 As Harshfield and Grim 34 recently summarized, the lesson that these animal models are examples of the "wrong" genes combined with the "wrong" environments needs to be extended to our research in human models of stress-related hypertension. This vision of stress-induced hypertension as requiring the wrong genes and the wrong environment offers a parsimonious explanation for inconsistencies in previous longitudinal investigations in humans.…”