Abstract
We have investigated hypertension-associated alterations in intracellular cations in the kidney by measuring intracellular pH, free Mg2+, free Ca2+, and Na+ concentrations in perfused normotensive and hypertensive rat (8-14 weeks old) kidneys using 31P, 19F, and double quantum-filtered (DQ) 23Na NMR. The effects of both anoxia and ischemia on the 23Na DQ signal confirmed its ability to detect changes in intracellular Na+. However, there was a sizable contribution of the extracellular Na+ to the 23Na DQ signal of the kidney. The intracellular free Ca2+ concentration, measured using 19F NMR and 5,5'difluoro-1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid, also increased dramatically during ischemia; the increase could be partly reversed by reperfusion. No significant differences were found between normotensive and hypertensive kidneys in the ATP level, intracellular pH, intracellular free Mg2+, and the 23Na DQ signal or in the extent of the extracellular contribution to the 23Na DQ signal. Oxygen consumption rates were also similar for the normotensive (5.02 +/- 0.46 mumol of O2/min/g) and hypertensive (5.47 +/- 0.42 mumol O2/min/g) rat kidneys. The absence of a significant difference in intracellular pH, Na+ concentration, and oxygen consumption between normotensive and hypertensive rat kidneys suggests that an alteration in the luminal Na+/H+ antiport activity in hypertension is unlikely. However, a highly significant increase (64%, p less than 0.01) in free Ca2+ concentration was found in perfused kidneys from hypertensive rats (557 +/- 48 nM, blood pressure = 199 +/- 5 mmHg, n = 6) compared with normotensive rats (339 +/- 21 nM, blood pressure = 134 +/- 6, n = 4) indicating altered renal calcium homeostasis in essential hypertension. An increase in intracellular free Ca2+ concentration without an accompanying change in the intracellular Na+ suggests, among many possibilities, that the Ca2+/Mg(2+)-ATPase may be inhibited in the hypertensive renal tissue.
Highlights
We have investigated hypertension-associatedalter- altered in hypertensive human leukocytes (e), and intracelations in intracellular cations in the kidney by meas- lularNa+concentration was reportedto be higherin the uring intracellular pH, free Mg2+,free Ca2+, and Na+ spontaneously hypertensive rat (SHR)' aorta (3)
No significant differences were found between nor- motensive and hypertensive kidneys in the ATP leve(l9,), demonstrated in rats of Dah1 salt-sensitive strain the Milan, and hypertensive SHR (11)in strain which intracellular pH, intracellular freeMg", and the23Na blood pressure in the recipientsof transplanted kidneys was double quantum-filtered (DQ) signal or in the extenotf the extracellular contri- determined by the genetic background of the donorkidney
No significant difference was mia, following anoxia, induced a DQ signal thatwas approx- detected in the intracellular free Mg2+ concentration, measimately %fold larger than thatobserved during anoxia, in the ured from the chemical shift difference between the a-and pabsence of Gd(PPPi)z
Summary
TheintracellularpH measuredfrom the measured upon quenching the extracellularcoherence with 2 chemical shift of the Pi resonance was not significantly mM Gd(PPPi)z- was approximately 5 times larger than the different between the normotensive (7.32 f 0.06) and hyperquenched DQ signalof the oxygenated control kidney. No significant difference was mia, following anoxia, induced a DQ signal thatwas approx- detected in the intracellular free Mg2+ concentration, measimately %fold larger than thatobserved during anoxia, in the ured from the chemical shift difference between the a-and pabsence of Gd(PPPi)z-. In these experiments thTevalue that phosphoryl resonances of ATP, between normotensive
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