GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Intrarenal ghrelin infusion stimulates distal nephron-dependent sodium reabsorption in normal rats.
Kemp. Brandon A BA; Howell. Nancy L NL; Gray. Jasmine T JT; Keller. Susanna R SR; Nass. Ralf M RM; Padia. Shetal H SH
Key Findings
- Ghrelin receptor mRNA is present in rat kidneys.
- Direct renal infusion of ghrelin sharply reduces urinary sodium excretion, indicating increased distal‑nephron sodium reabsorption.
- The ghrelin‑receptor antagonist D‑Lys‑3‑GHRP‑6 blocks the sodium‑retaining effect of ghrelin and on its own raises sodium excretion.
Practical Outcomes
- If you use ghrelin‑mimicking peptides like GHRP‑6 for growth‑hormone or performance purposes, they may also cause your body to retain sodium, which could affect blood pressure and fluid balance. Monitoring electrolytes and blood pressure is advisable, and any attempts to counteract this effect would need a specific ghrelin‑receptor blocker, which is not commonly used outside research.
Summary
The study shows that kidneys have ghrelin receptors and that giving ghrelin directly to the kidney makes the organ reabsorb more sodium, lowering how much sodium ends up in the urine. This sodium‑saving effect can be blocked by a specific ghrelin‑receptor blocker (D‑Lys‑3‑GHRP‑6), which by itself makes the kidneys dump more sodium.
Abstract
Ghrelin is a 28-amino acid peptide hormone that exerts powerful orexigenic effects. Ghrelin receptor expression has been reported in the kidney, but the role of ghrelin in the kidney is unknown. The present studies confirmed ghrelin receptor mRNA expression in the kidneys of normal Sprague Dawley rats (n=6) using reverse transcription polymerase chain reaction (PCR) and sequencing of the 588-bp PCR product. To test intrarenal ghrelin action, uninephrectomized rats received 3 cumulative 1-hour renal interstitial (RI) infusions of 5% dextrose in water (vehicle, n=21), ghrelin (n=10), ghrelin plus specific ghrelin receptor antagonist [D-Lys-3]-GHRP-6 (n=24), or [D-Lys-3]-GHRP-6 alone (n=32). Mean arterial pressure (MAP), urine sodium excretion rate (U(Na)V), glomerular filtration rate (GFR), fractional excretion of sodium (FE(Na)), and fractional excretion of lithium (FE(Li)) were calculated for each period. RI ghrelin infusion significantly decreased U(Na)V to 86 ± 4.9% (P<0.05), 74 ± 6.5% (P<0.01), and 62 ± 10% (P<0.01) of baseline during periods 1 to 3, respectively. Ghrelin also significantly decreased FE(Na) to 68 ± 11% (P<0.05), 57 ± 8.6% (P<0.001), and 59 ± 12% (P<0.01) of baseline, without changing GFR or FE(Li). Identical ghrelin infusions in the presence of [D-Lys-3]-GHRP-6 failed to permit reductions in U(Na)V or FE(Na). Following [D-Lys-3]-GHRP-6 infusion alone, U(Na)V increased from 0.06 ± 0.01 to 0.18 ± 0.03 μmol/min (P<0.0001). Concomitant increases in FE(Na) were also observed (0.23 ± 0.03% to 0.51 ± 0.06% [P<0.001]), without changes in MAP, GFR, or FE(Li). Together, these data introduce a novel intrarenal ghrelin-ghrelin receptor system, which, on activation, significantly increases Na(+) reabsorption at the level of the distal nephron.
Study Information
pubmed
2011
2011-01-10T00:00:00.000Z
10.1161/hypertensionaha.110.166413