Blood pressure in streptozotocin-treated Brattleboro and Long-Evans rats

Abstract

The diabetogenic agent streptozotocin (STZ) was injected intraperitoneally in Long-Evans and arginine vasopressin (AVP)-deficient Brattleboro rats. Twenty-eight days later both strains had a bradycardia and systolic hypotension; STZ-treated Brattleboro rats also had diastolic hypotension. The vasopressin (V1-receptor) antagonist, d(CH2)5[Tyr(Et)]DAVP, had no effect on resting blood pressure (BP) or heart rate (HR) in either strain of rat, indicating the relative maintenance of diastolic BP in STZ-treated Long-Evans rats was not dependent on acute vascular actions of AVP. Captopril caused a modest hypotension in all groups of rats, indicating that BP was not differentially dependent on the renin-angiotensin system in the different groups. In the presence of captopril and the ganglion blocker, pentolinium tartrate, the AVP-mediated recovery in BP was impaired in STZ-treated Long-Evans rats. During administration of d(CH2)5[Tyr(Et)]DAVP and pentolinium, the angiotensin II (ANG II)-mediated BP recovery was smaller in both groups of STZ-treated rats, indicating that this abnormality was not likely to be caused by inhibition of renin release by AVP. The abnormalities in ANG II- and AVP-mediated recovery were prevented by insulin treatment.

The effects of endothelin‐1 and NG‐nitro‐l‐arginine methyl ester on regional haemodynamics in conscious rats with streptozotocin‐induced diabetes mellitus

“…Thus, elevated circulating vasopressin levels causing coronary vasoconstriction (Boyle & Segel, 1986), or interactions between vasopressin and cardiac neural control (Osborn et al, 1987), are not likely to be responsible for the bradycardia. Clearly, activation of vagal mechanisms (Kofo-Abayomi & Lucas, 1987) and/or inhibition of sympathetic efferent input to the heart, independent of vasopressin, could explain the slow sinus rate following treatment with STZ, but the bradycardia has been found to persist following ganglion blockade (Hebden et al, 1987a;Tomlinson et al, 1990). This observation indicates that myocardial factors (Savarese & Berkowitz, 1979;Dillman, 1982;Ganguly et al, 1983;Sundaresan et al, 1984) may be responsible for the bradycardia in STZ-treated rats.…”

“…Stuesse et al, 1982;Carbonell et al, 1987;Hebden et al, 1987a;Tomlinson et al, 1989;1990). Tomlinson et al (1990) have shown that Brattleboro (i.e. vasopressin-deficient) rats have a bradycardia following treatment with STZ.…”

Regional and cardiac haemodynamic responses to glyceryl trinitrate, acetylcholine, bradykinin and endothelin‐1 in conscious rats: effects of NG‐nitro‐l‐arginine methyl ester

“…Elsewhere we have shown the combination of these doses of pentolinium, captopril and d(CH2)5[Tyr- (Et)]DAVP blocks all endogenous factors contributing to blood pressure recovery in conscious, Long Evans rats (Tomlinson et al, 1990). Hence, these experiments were designed to abolish any possible contributions of baroreflex on neurohumoral mechanisms to the responses evoked by glyceryl trinitrate, acetylcholine, bradykinin and endothelin-1.…”

Aminoguanidine reduces regional albumin clearance but not urinary albumin excretion in streptozotocin-diabetic rats

“…In addition, one study does not report effects on blood pressure [30] whereas the other refers to blood pressures that were determined by indirect tail-cuff plethysmography, and therefore cannot be interpreted properly. There is strong evidence that this method produces artificially elevated blood pressure recordings, as a result of either structural or haemodynamic alterations in the tail of diabetic rats [17,18]. In our own laboratory we also observed differences between direct intra-arterial blood pressure measurements and tail-cuff recordings.…”

“…Since it has been shown that blood pressure data obtained with the indirect tall-cuff method are unreliable and artificially elevated in diabetic rats [17,18], blood pressure was measured di-…”