PubMed Health⌕ Search

Biomedical subjects

M Blankenship

Publications and source records attributed to M Blankenship.

6 recordsLinked to original sources
PubMed1998

Atrial natriuretic peptide increases urodilatin in the circulation.

BACKGROUND: Urodilatin is a 32-amino-acid (AA) peptide formed in the kidney. METHODS: High-performance gel permeation chromatography and high-pressure liquid chromatography evaluation of plasma followed by sensitive urodilatin and atrial natriuretic peptide (ANP) assays revealed that urodilatin does circulate distinctly from ANP. RESULTS: Urodilatin circulates at very low levels (i.e 9-12 pg/ml). Infusion of ANP increased the circulating concentration of urodilatin 135-fold (p < 0.001), suggesting that some of the effects of ANP may be mediated by urodilatin while long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide did not affect urodilatin in healthy humans (n = 30). Only ANP decreased the renal clearance of urodilatin (60-75%, p < 0.01). Urodilatin was metabolized into peptides smaller than 5 AAs as well as excreted intact into urine. CONCLUSION: Urodilatin circulates and is increased by ANP in humans.

Adult↗
PubMed1996

Atrial natriuretic peptide increases adrenomedullin in the circulation of healthy humans.

Adrenomedullin (ADM) is a new 52 amino acid peptide originally isolated from extracts of human pheochromocytoma. ADM's biologic properties are nearly identical to those of atrial natriuretic peptides. Thus, the 4 peptide hormones originating from amino acids 1-30 [long acting natriuretic peptide], 31-67 [vessel dilator], 79-98 [kaliuretic peptide] and 99-126 [atrial natriuretic factor; ANF] of the 126 amino acid ANF prohormone as well as ADM have blood pressure lowering and diuretic properties. The present investigation was designed to determine if one or more of these 4 atrial natriuretic peptides increase adrenomedullin within the circulation of healthy humans. Infusion of 100 ng/kg body weight/minute for 60 minutes of the respective atrial peptides resulted in a 4-fold (P < 0.001) increase in the circulating concentration of adrenomedullin secondary to the ANF infusion but no increase in adrenomedullin with the long acting natriuretic peptide, vessel dilator, or kaliuretic peptide infusions. The four-fold increase of adrenomedullin in the circulation persisted throughout the infusion of ANF, but returned to pre-infusion levels within 30 minutes of stopping the ANF infusion. Infusion of 10 pg/kg body weight/minute for 60 minutes of ANF resulted in a 2 1/2-fold increase (P < 0.05) in the circulating concentration of adrenomedullin. There was a significant (P < 0.01) diuresis and blood pressure lowering effect with each of the atrial natriuretic peptides in the present investigation. This investigation suggests that 1) atrial natriuretic factor increases the release of adrenomedullin and 2) that the diuretic and blood pressure lowering effects previously attributed to atrial natriuretic factor may be partially due to adrenomedullin since both increased during the ANF infusion and both have similar biologic effects. As opposed to atrial natriuretic factor, adrenomedullin was not increased by long acting natriuretic peptide, vessel dilator, or kaliuretic peptide suggesting that their biologic effects do not involve adrenomedullin.

Adrenomedullin↗
PubMed1985

Disruption of myelin sheaths in mouse brain in vitro and in vivo by staphylococcal alpha-toxin.

In recent studies we have demonstrated that staphylococcal alpha-toxin can specifically bind to rabbit vagus nerves and cause disruption of myelin sheaths in this peripheral nerve in vitro. We report here that staphylococcal alpha-toxin, incubated in vitro with brain slices or injected intracerebrally into mice, can induce disruption of myelin sheaths in central nervous tissue. Intracerebral injection of alpha-toxin is followed by a characteristic and reproducible syndrome involving ataxia followed by a severe contraction of the limbs on the side contralateral to the injection and a maximal extension of the opposing limbs. At 1.1 micrograms of toxin injected, death occurs within 20 min. Histopathologic examination reveals extensive demyelination with minimal involvement of the axons. It is possible that staphylococcal alpha-toxin may play a role in the etiology of multiple sclerosis.

Animals↗