Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

Kaufman, James S.; Peck, Michael J.; Hamburger, Robert J.; Flamenbaum, Walter

doi:10.1159/000183830

Cited by 4 publications

(2 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies in animal models and in humans indicate that aldosterone stimulates renal synthesis and urinary excretion of kallikrein (Margolius et al, 1974;Fejes-Toth and Naray-Fejes-Toth, 1984;Kaufman et al, 1986;Albano et al, 1994). In this study, as in previous studies, urinary kallikrein excretion during low salt intake correlated with serum aldosterone concentrations.…”

supporting

confidence: 80%

Loss of Sodium Modulation of Plasma Kinins in Human Hypertension

Murphey

Eccles²,

Williams³

et al. 2004

J Pharmacol Exp Ther

View full text Add to dashboard Cite

We studied the effect of salt intake and hypertension on the systemic kallikrein-kinin system (KKS), as measured by bradykinin (BK) 1-5, a stable circulating bradykinin metabolite, and the tissue KKS, as measured by urinary kallikrein excretion. Venous BK 1-5, urinary kallikrein, and components of the reninangiotensin-aldosterone system were measured in 35 normotensive and 19 hypertensive subjects who were maintained on a high (200 mmol/day) or low (10 mmol/day) salt diet. Salt restriction decreased mean arterial pressure (MAP) (P Ͻ 0.001 overall) and the plasma angiotensin-converting enzyme (P ϭ 0.017) and increased plasma renin activity (P Ͻ 0.001) and serum aldosterone (P Ͻ 0.001). There was an interactive effect of salt intake and hypertension on plasma BK 1-5 (P ϭ 0.043), with BK 1-5 significantly lower during low compared with high salt intake in normotensive (24.7 Ϯ 2.6 versus 34.9 Ϯ 5.6 fmol/ml, P ϭ 0.002) but not hypertensive subjects (30.6 Ϯ 4.6 versus 27.5 Ϯ 2.8 fmol/ml, P ϭ 0.335). In normotensives, the change in plasma BK 1-5 from high to low salt intake correlated with the change in MAP (r ϭ 0.533, P ϭ 0.004). Urinary kallikrein was higher during low compared with high salt intake (P Ͻ 0.001) in both groups. There was no effect of salt intake on urinary BK 1-5. In summary, the systemic and renal KKSs act in tandem to modulate the response to salt intake. The systemic system is activated during high salt intake and counterbalances increased vascular response to pressors. With sodium restriction, the renal system is activated and counterbalances the increased sodium-retaining state induced by activation of the renin-angiotensin-aldosterone system. With hypertension, these modulating effects are diminished or lost, supporting a role for both systems in the development/maintenance of hypertension.

show abstract

supporting

confidence: 80%

Loss of Sodium Modulation of Plasma Kinins in Human Hypertension

Murphey

Eccles²,

Williams³

et al. 2004

J Pharmacol Exp Ther

View full text Add to dashboard Cite

show abstract

“…The creatinine concentration was determined by an automated enzymatic assay, and Na + and K + concentrations in plasma and urine were determined using an electrode (automatic analyzer 7350, Hitachi, Japan). Plasma aldosterone levels were measured by radioimmunoassay [12].…”

Section: Chemical Measurements On Blood and Urine Samplesmentioning

confidence: 99%

A low-Na + diet enhances expression of mRNA for epithelial Na + channel in rat renal inner medulla

Ono

Kusano

Muto

et al. 1997

Pfl�gers Archiv European Journal of Physiology

View full text Add to dashboard Cite

The purpose of the present study was to determine whether the renal inner medulla expresses mRNA for the rat epithelial Na + channel (rENaC) and, if so, to define its regulatory properties using a low-Na + diet model. We detected α, β and γ subunit mRNA in rat renal inner medulla using reverse transcriptase-polymerase chain reaction (RT-PCR) with primers specific for rENaC α, β and γ subunits. Moreover, we have developed a specific probe for the α subunit using RT-PCR with rENaC α-subunit-specific primers. The resulting cDNA was verified by sequencing and was then used in Northern blot analysis of distal colon, whole kidney and inner medulla. The probe for the rENaC α subunit hybridized not only to distal colon RNA but also to inner medulla RNA derived from rats fed a normal diet. Furthermore, we examined the effect of a low-Na + diet on α, β and γ subunit mRNA expression of rENaC using fulllength cDNA as a probe. A marked elevation of rENaC α subunit mRNA abundance in the inner medulla was observed in response to a high plasma aldosterone concentration induced by dietary Na + deprivation. On the other hand, neither β nor γ subunit mRNA expression was enhanced by a low-Na + diet. From these results, it is suggested that rENaC is responsible for Na + transport in the renal inner medulla and that is probably regulated via transcriptional control of the α subunit of ENaC.

show abstract

Adrenocortical Response to Critical Illness

Jagger¹

1997

Endocrinology of Critical Disease

View full text Add to dashboard Cite

Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

Cited by 4 publications

References 26 publications

Loss of Sodium Modulation of Plasma Kinins in Human Hypertension

Loss of Sodium Modulation of Plasma Kinins in Human Hypertension

A low-Na + diet enhances expression of mRNA for epithelial Na + channel in rat renal inner medulla

Adrenocortical Response to Critical Illness

Contact Info

Product

Resources

About