The effect of norepinephrine on aortic 42K turnover during deoxycorticosterone acetate hypertension and antihypertensive therapy in the rat.

Jones, Allan W.; Sander, Paulina; Kampschmidt, D L

doi:10.1161/01.res.41.2.256

Cited by 20 publications

(9 citation statements)

References 13 publications

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“…Histological examination of tissue slices from kidneys denervated in this manner showed that there was no catecholamine fluorescence at 6 weeks postdenervation. It has also been shown that an intact sympathetic nervous system was not a requirement for the development of an increased responsiveness to NE or an increased potassium turnover in aortae from DOCA hypertensive rats (Jones et al, 1977).…”

Section: Peripheral Sympathectomymentioning

confidence: 99%

Significance of sodium, sympathetic innervation, and central adrenergic structures on renal vascular responsiveness in DOCA-treated rats.

Berecek¹,

Murray²,

Gross³

1980

Circulation Research

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SUMMARY The effects of sodium, sympathetic innervation, and central adrenergic structures on the development of changes in renal vascular reactivity were studied in unilaterally nephrectomized rats treated with a single implant of deoxycorticosterone acetate (DOCA; 100 mg/kg). Vascular reactivity to norepinephrine (NE) and vasopressin (ADH) was assessed in isolated kidneys perfused with a synthetic medium. Influence of sodium was determined by placing DOCA-treated rats on high, normal, and low sodium intakes. Neural influence was studied by means of local denervation of the renal artery and by intravenous (iv) and intraventricular (ivt) administration of 6-hydroxydopamine (6-OHDA). Marked changes in renal vascular reactivity in DOCA-treated rats were already apparent prior to the rise in blood pressure. Dose-response curves for NE and ADH showed parallel leftward shifts and decreased threshold doses. Normal sodium intake, local denervation, and peripheral sympathectomy had no effect on the development of these vascular changes in DOCA-treated rats. However, sodium deficiency and ivt administration of 6-OHDA totally prevented development of enhanced vascular reactivity. These results imply that increased vascular reactivity is a major factor in the development of DOCA-hypertension. Circ Res 47: 675-683, 1980

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Section: Peripheral Sympathectomymentioning

confidence: 99%

Significance of sodium, sympathetic innervation, and central adrenergic structures on renal vascular responsiveness in DOCA-treated rats.

Berecek¹,

Murray²,

Gross³

1980

Circulation Research

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“…The response to a given dose of NE, Ak, was taken as the difference between the highest rate constant in the presence of the agonist and the rate constant for the wash period just before exposure to NE. The maximal response, Ak,,,, was taken as the response to a supramaximal dose of NE, 6 X 1 O-' M (9). The individual responses, Ak, were normalized in terms of Akmax for each aorta and represented as percentage.…”

Section: Methods Animal and Tissue Preparationmentioning

confidence: 99%

“…Increased blood and plasma volume (3), elevated levels of an adrenal mineralocorticoid, 1 80H-DOC (4), and hyperresponsiveness to intravenous injection of various pressor agents (5-7) have been reported in the hypertensive S rat when compared to normotensive controls. In models of hypertension induced by mineralocorticoid plus salt (8)(9)(10) as well as the SHR (spontaneously hypertensive rat) form of genetic hypertension ( 1 I), norepinephrine supersensitivity has been associated with altered ionic transport in vascular smooth muscle. It is feasible, then, that the vascular smooth muscle of the genetically salt-sensitive Dahl S rat may exhibit similar ionic transport alterations.…”

mentioning

confidence: 99%

“…Using 42K efflux as a measure of potassium turnover, an increase in the basal 42K turnover and response to norepinephrine have been found in rats made hypertensive by treatment with salt plus deoxycorticosterone acetate (DOCA) or aldosterone (8)(9)(10). The purpose of the present study was to assess the basal 42K turnover and its response to norepinephrine in the vascular smooth muscle of the Dahl rat.…”

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confidence: 99%

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Potassium Turnover and Norepinephrine Sensitivity in the Thoracic Aorta of the Dahl Rat

Smith

Jones

1983

Experimental Biology and Medicine

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This in vitro study evaluated the basal 42K turnover and response to norepinephrine (NE) in the thoracic aorta removed from Dahl salt-sensitive (S) and salt-resistant (R) rats. Fiveweek-old S and R rats were placed on either a high-salt (HS) or low-salt (LS) diet. After 5 weeks of the diet, systolic blood pressure, aortic weight/length ratio, and the cellular pool of K+ were elevated in the S-HS group only. In contrast, the steady state turnover of 42K, the NE EDSo, and the response to a supramaximal dose of NE were the same in both groups of salt-sensitive and salt-resistant rats. These results suggest that, despite the presence of a greatly elevated systolic blood pressure and evidence of aortic hypertrophy, the intrinsic electrolyte metabolism of the vascular smooth muscle in the Dahl hypertensive rat is the same as that of the Dahl normotensive rat.29 I

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“…8 Membrane supersensitivity to norepinephrine (NE) also occurs during mineralocorticoid hypertension in rats as measured by agonist-induced increases in 42 K efflux. 9 l0 This supersensitivity may extend to several types of agonists including peptides and indicates that a relatively nonspecific supersensitivity develops." It is not clear whether the development of drug supersensitivity is closely related to the alteration in resting fluxes, or whether it results from altered receptor syn-thesis, control, and transduction with membrane channels.…”

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Temperature dependence of ionic transport and norepinephrine stimulation of rat aorta during DOCA hypertension.

Warden¹,

Jones²

1984

Hypertension

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SUMMARY Temperature perturbation was used to determine whether increased turnover of Na, K, and Cl at 37° C in aortas from rats made hypertensive with deoxycorticosterone acetate salt treatment (DOCH) reflects an increased number of transport sites that individually maintain relatively normal function. Decreasing temperature reduced the resting effluxes of 42 K, ^Cl, and M Na (active and passive) from control and DOCH in parallel fashion. The slope of the Arrhenius plots (activation energies) and the transition temperatures at which major changes in slope occurred were similar in controls and DOCH. In contrast to the results for resting effluxes, the temperature dependence for the effects of norepinephrine (NE) on contraction and on K and "^Cl effluxes in DOCH differed from controls. At 20° C, the responses to NE were either abolished or greatly suppressed in DOCH, as compared to controls, while no significant differences between the two groups were observed at 30° C. These results indicate that alterations in resting 42 K, -"Cl, and 24 Na effluxes in DOCH may result from an increased number of transport sites in the membranes of vascular smooth muscle. The concept that alterations occurred in the integral components of the membrane is also supported by the observation that increased resting 42 K and Cl effluxes in DOCH at 37° C persisted in aortas that had undergone cold storage for 2 days before incubation at 37° C. The altered temperature dependence for the effects of NE on DOCH, compared to controls, indicates that the involvement of agonist-receptor-membrane events may be dissociated from the alterations in resting ionic fluxes. K occurred in the aorta and femoral arteries from rats made hypertensive either with deoxycorticosterone acetate (DOCA) or aldosterone.1 -2 The net exchange of cellular Na and K in tail arteries for extracellular Li also proceeded at a faster rate in DOCA hypertensive rats.3 One important consequence of such alteration would be to increase the leak of ions along their electrochemical gradient, which would lead to altered excitability. In addition to these passive movements, evidence exists for an inFrom the Department of Physiology, University of Missouri at Columbia, Columbia, Missouri 65212.

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The effect of norepinephrine on aortic 42K turnover during deoxycorticosterone acetate hypertension and antihypertensive therapy in the rat.

Cited by 20 publications

References 13 publications

Significance of sodium, sympathetic innervation, and central adrenergic structures on renal vascular responsiveness in DOCA-treated rats.

Significance of sodium, sympathetic innervation, and central adrenergic structures on renal vascular responsiveness in DOCA-treated rats.

Potassium Turnover and Norepinephrine Sensitivity in the Thoracic Aorta of the Dahl Rat

Temperature dependence of ionic transport and norepinephrine stimulation of rat aorta during DOCA hypertension.

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