Effects of hypoxia on carotid body dopamine content and release in developing rabbits.

Hypoxia induces dopamine (DA) release from the carotid body (CB), but the role of DA during hypoxia in the postnatal maturation of carotid chemosensory discharge remains controversial. The aim of this study was to evaluate changes in CB content and release of DA evoked by hypoxia at different stages of development in the rabbit. Five groups of rabbits aged < or = 24 h (n = 9), 5 days (n = 27), 15 days (n = 18), 25 days (n = 16), and > or = 1 yr (n = 11) were studied. CBs were surgically removed and immediately incubated at 37 degrees C for 1 h in a surviving medium equilibrated with 100% O2 or 8% O2 in N2. The content of DA in the CB ([DA]CB) and the DA released in the surviving medium ([DA]r) were measured by high-performance liquid chromatography. [DA]CB was significantly larger in adults than in all pup groups in both 100% O2 [385.5 +/- 74.1 (SE) pmol/CB in adults and 43.6 +/- 6.0 pmol/CB in pups; P < 0.01] and hypoxia (518.1 +/- 99.9 pmol/CB in adults and 24.7 +/- 3.2 pmol/CB in pups; P < 0.01), presumably because of the larger CB mass. [DA]r was significantly larger in hypoxia than in 100% O2 only in 25-day-old rabbits (19.8 +/- 4.2 and 3.6 +/- 1.1 pmol/h, respectively; P < 0.01) and in adults (183.9 +/- 57.7 and 7.9 +/- 1.7 pmol/h, respectively; P < 0.01). The average ratio of [DA]r in hypoxia to [DA]r in 100% O2 ranged from 1.3 to 2.2 in the three younger age groups and was 5.5 and 23.3 in 25-day-old and adult rabbits, respectively. We conclude that the release of DA evoked by hypoxia is weak at birth and develops during the first weeks of life in rabbits.

Potassium-argon dating of the cape granite and a granitized xenolith at sea point.

Ages obtained by potassium-argon dating are reported for the total rock, light mineral fraction and heavy mineral fractions of the Cape Granite, and of a granitized xenolith derived from the Malmesbury sediments. These ages lie between 430 and 554 million years. The heavy mineral fractions from each rock type show the oldest age, 540 (granite) and 554 (xenolith) million years. These ages are interpreted as lower limits, and the granite age confirms the age of 553 million years found by rubidium-strontium dating. The coincidence of the ages of the different fractions of the granite and xenolith samples is discussed in the light of the different suggestions about the age of the Malmesbury sediments. The conclusion is reached that all pre-granitization history has been eliminated. The possibility of the use of argon retention as a measure of metamorphic activity is suggested.

Carotid body dopamine content and release by short-term hypoxia: effect of haloperidol and alpha methyl paratyrosine.

Dopamine (DA) is thought to modulate the transduction of the hypoxic stimulus by the glomus cell in the carotid body (CB). The hypothesis tested here is that presynaptic DA D2 receptors (D2's) located on the type 1 cell function as autoreceptors to control DA release and/or synthesis. The aim of the study was to compare the effects of blocking D2's with haloperidol and DA synthesis with alpha methyl paratyrosine (AMPT) on the in vitro carotid body DA response to hypoxia. 54 CB's sampled from adult rabbits were incubated for one hour in a surviving medium bubbled with either 100% O2 or 8% O2 Sixteen CB's served as control (100% O2: n = 8, 8% O2: n = 8), 18 (100% O2: n = 8, 8% O2: n = 10) were sampled from rabbits pretreated with AMPT and 20 (100% O2: n = 12, 8% O2: n = 8) were incubated with micromolar concentrations of haloperidol. At the end of exposure. DA contained in the carotid body (DACB) and released in the surviving medium (DAr) were measured by HPLC. In 100% O2 DACB was not different between either AMPT or haloperidol and control, but DAr was significantly higher in the haloperidol group compared with control (mean +/- SE: 26.6 +/- 7.4 versus 7.6 +/- 2.0 pmol/h, P < 0.02). In 8% O2, control DACB (576 +/- 133 pmol/CB) was significantly higher than AMPT or haloperidol (respectively 228 +/- 29.6 and 246 +/- 49.9 pmol/CB, P < 0.01) and control DAr (234 +/- 72.3 pmol/h) was also significantly higher than AMPT or haloperidol (respectively 28.8 +/- 5.2 and 40.6 +/- 11.4 pmol/h, P < 0.01). Finally, DAr was significantly larger in 8% O2 than in 100% O2 in control and AMPT groups (P < 0.01), but not in the haloperidol group. The increase in DAr by haloperidol in the resting CB is consistent with the blockade of D2's regulating DA release. The decreased DAr in 8% O2 after AMPT suggests that increased DA synthesis contributes to maintain DA secretion by the type I cell exposed to short term hypoxia. The lack of difference in DAr between 8% O2 and 100% O2 after haloperidol probably reflects non specific--i.e., D2 independent--effect of micromolar concentration of haloperidol on DA synthesis and/or sodium-calcium exchangers during hypoxia.