TY - JOUR

T1 - Mechanisms of pH control in the midgut of Lutzomyia longipalpis

T2 - Roles for ingested molecules and hormones

AU - Santos, Vânia C.

AU - Nunes, Cássio A.

AU - Pereira, Marcos H.

AU - Gontijo, Nelder F.

PY - 2011/5/1

Y1 - 2011/5/1

N2 - Control of the midgut pH in Lutzomyia longipalpis enables the insect's digestive system to deal with different types of diet. Phlebotomines must be able to suddenly change from a condition adequate to process a sugar diet to one required to digest blood. Prior to blood ingestion, the pH in the midgut is maintained at ∼6 via an efficient mechanism. In the abdominal midgut, alkalization to a pH of ∼8 occurs as a consequence of the loss of CO 2 from blood (CO2 volatilization) and by a second mechanism that is not yet characterized. The present study aimed to characterize the primary stimuli, present in the blood, that are responsible for shutting down the mechanism that maintains a pH of 6 and switching on that responsible for alkalization. Our results show that any ingested protein could induce alkalization. Free amino acids, at the concentrations found in blood, were ineffective at inducing alkalization, although higher concentrations of amino acids were able to induce alkalization. Aqueous extracts of midgut tissue containing putative hormones from intestinal endocrine cells slightly alkalized the midgut lumen when applied to dissected intestines, as did hemolymph collected from blood-fed females. Serotonin, a hormone that is possibly released in the hemolymph after hematophagy commences, was ineffective at promoting alkalization. The carbonic anhydrase (CA) enzyme seems to be involved in alkalizing the midgut, as co-ingestion of acetazolamide (a CA inhibitor) with proteins impaired alkalization efficiency. A general model of alkalization control is presented.

AB - Control of the midgut pH in Lutzomyia longipalpis enables the insect's digestive system to deal with different types of diet. Phlebotomines must be able to suddenly change from a condition adequate to process a sugar diet to one required to digest blood. Prior to blood ingestion, the pH in the midgut is maintained at ∼6 via an efficient mechanism. In the abdominal midgut, alkalization to a pH of ∼8 occurs as a consequence of the loss of CO 2 from blood (CO2 volatilization) and by a second mechanism that is not yet characterized. The present study aimed to characterize the primary stimuli, present in the blood, that are responsible for shutting down the mechanism that maintains a pH of 6 and switching on that responsible for alkalization. Our results show that any ingested protein could induce alkalization. Free amino acids, at the concentrations found in blood, were ineffective at inducing alkalization, although higher concentrations of amino acids were able to induce alkalization. Aqueous extracts of midgut tissue containing putative hormones from intestinal endocrine cells slightly alkalized the midgut lumen when applied to dissected intestines, as did hemolymph collected from blood-fed females. Serotonin, a hormone that is possibly released in the hemolymph after hematophagy commences, was ineffective at promoting alkalization. The carbonic anhydrase (CA) enzyme seems to be involved in alkalizing the midgut, as co-ingestion of acetazolamide (a CA inhibitor) with proteins impaired alkalization efficiency. A general model of alkalization control is presented.

KW - Ingested nutrient

KW - Insect hormone

KW - Lutzomyia longipalpis

KW - Midgut alkalization

KW - Midgut pH control

U2 - 10.1242/jeb.051490

DO - 10.1242/jeb.051490

M3 - Journal article

C2 - 21490249

AN - SCOPUS:79955001660

VL - 214

SP - 1411

EP - 1418

JO - Journal of Experimental Biology

JF - Journal of Experimental Biology

SN - 0022-0949

IS - 9

ER -