Aldosterone and helminths (especially nematodes/whipworms/roundworms)
Dogs and cats infested with whipworms often present with pseudo-hypoaldosteronism (faux aldosterone deficiency). All symptoms of aldosterone defiency are present but the animals have high to normal plasma serum aldosterone levels (shown in quote 1). Once the parasite infestation is cleared, the pseudo-hypoaldosteronism resolves. This suggests that the whipworm infestation is somehow blocking the action of aldosterone.
Whipworms excrete neurokinin B to hide themselves from host immune system. Interestingly and possibly relevant to pg related ms remission, the human placenta releases the same tachykinin to hide itself from mom's immune system.
Neurokinin B stimulates the secretion of luteinizing hormone (in sheep, as show in quote 2).
Luteinizing hormone is secreted in both men and women from the pituitary gland and stimulates the production of progesterone (a step in testosterone production for men).
Progesterone blocks aldosterone receptors.
Basal and ACTH-Stimulated Plasma Aldosterone Concentrations are Normal or Increased in Dogs With Trichuriasis-Associated Pseudohypoadrenocorticismhttp://endo.endojournals.org/content/151/8/3836.short
Thomas K. Graves1,†,
William D. Schall1,
Raymond F. Nachreiner2
Article first published online: 28 JUN 2008
We measured plasma concentrations of Cortisol and aldosterone before and after administration of adrenocorticotropin (ACTH) in dogs with trichuriasis. These dogs had physical examination, historical, and serum electrolyte findings suggestive of hypoadrenocorticism; trichuriasisassociated pseudohypoadrenocorticism has been reported previously. We found normal basal and ACTH-stimulated plasma Cortisol concentrations. Basal and ACTH-stimulated plasma aldosterone concentrations were normal in 2 dogs and increased in 3 dogs, suggesting that the electrolyte abnormalities seen in this clinical syndrome are not due to aldosterone deficiency.
Neurokinin B Acts via the Neurokinin-3 Receptor in the Retrochiasmatic Area to Stimulate Luteinizing Hormone Secretion in Sheep
Heather J. Billings,
John M. Connors,
Stephanie N. Altman,
Stanley M. Hileman,
Michael N. Lehman,
Christina J. McManus,
Casey C Nestor,
Britni H. Jacobs and
Robert L. Goodman
- Author Affiliations
Departments of Neurobiology and Anatomy (H.J.B.) and Physiology and Pharmacology (J.M.C., S.N.A., S.M.H., I.H., C.J.M.; C.CN., B.H.J., R.L.G.), Robert C. Byrd Health Sciences Center, Morgantown, West Virginia 26506-9128; and Department of Anatomy and Cell Biology (M.N.L.), Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Address all correspondence and requests for reprints to: Heather J. Billings, Ph.D., Department of Neurobiology and Anatomy, West Virginia University, Health Sciences Center, P.O. Box 9128, Morgantown, West Virginia 26506-9128. E-mail: firstname.lastname@example.org
Recent data have demonstrated that mutations in the receptor for neurokinin B (NKB), the NK-3 receptor (NK3R), produce hypogonadotropic hypogonadism in humans. These data, together with reports that NKB expression increases after ovariectomy and in postmenopausal women, have led to the hypothesis that this tachykinin is an important stimulator of GnRH secretion. However, the NK3R agonist, senktide, inhibited LH secretion in rats and mice. In this study, we report that senktide stimulates LH secretion in ewes. A dramatic increase in LH concentrations to levels close to those observed during the preovulatory LH surge was observed after injection of 1 nmol senktide into the third ventricle during the follicular, but not in the luteal, phase. Similar increases in LH secretion occurred after insertion of microimplants containing this agonist into the retrochiasmatic area (RCh) in anestrous or follicular phase ewes. A low-dose microinjection (3 pmol) of senktide into the RCh produced a smaller but significant increase in LH concentrations in anestrous ewes. Moreover, NK3R immunoreactivity was clearly evident in the RCh, although it was not found in A15 dopaminergic cell bodies in this region. These data provide evidence that NKB stimulates LH (and presumably GnRH) secretion in ewes and point to the RCh as one important site of action. Based on these data, and the effects of NK3R mutations in humans, we hypothesize that NKB plays an important stimulatory role in the control of GnRH and LH secretion in nonrodent species.