Catanzaro O L, Vila S B, Martinez Seeber A
Pharmacol Res Commun. 1985 Aug;17(8):725-32. doi: 10.1016/0031-6989(85)90089-x.
The effects of furosemide and captopril were studied in nephrectomized rats with and without submaxillary gland. Captopril increased blood flow, but did not modified blood pressure. Furosemide plus captopril decreased significantly blood pressure. These results suggest a release of kallikrein by furosemide and probably a formation of kinin from plasma kininogen. On the other hand, rats sialodectomized showed no alterations in blood pressure in response to both drugs. These data suggest that submaxillary gland kallikrein participates in the mechanism of blood pressure regulation and blood flow of the gland at least in our experimental conditions. Glandular kallikreins are serine proteases which release kinins from substrates called kininogen. They are found in extracts and secretions of all exocrine glands. This proteases have been implicated in the regulation of exocrine glands and kidney blood flow, in water and electrolyte balance, in blood pressure regulation and in the pathogenesis of experimental and clinical hypertension (Carretero et al., 1978; Martinez Seeber et al., 1982). Glandular kallikreins of exocrine glands and kidney are secreted into the exocrine secretions and urine and also into the vascular compartment, where a local blood flow could be affected. According to Gautvik et al. (1980), rat submandibular gland is an organ rich in kallikrein, and significants amounts of the gland enzyme are release into the circulation after stimulation (Orstavik et al., 1982). Hilton and Lewis (1956) first proposed that glandular kallikrein-kinin system in salivary glands regulates vasodilation, probably through the effect of kallikrein on plasma kininogen.(ABSTRACT TRUNCATED AT 250 WORDS)
