The population and community structure of Hawaiian fringing-reef crustose Corallinaceae (Rhodophyta,Cryptonemiales)

Measurements of cover, relative density, and frequency are given for the major reefbuilders on the Waikiki fringing reef. Crustose coralline algae cover 39% of the reef surface and exceed all other organisms as the major builders and consolidators of reef materials. An unidentified coralline (melobesioid C) covers the greatest area (17 %), but Hydrollthon reinboldii (Weber-van Bosse & Foslie) Foslie (11 % cover) because of its thicker thalli and higher relative density (45 %) and frequency (68 %) values is the primary limestone former. Melobesioid C ranks second and Sporolithon erythraeum (Rothpletz) Kylin (6 % cover) third in relative importance. Porolithon onkodes (Heydrich) Foslie (3 % cover), although shown by its low density (4 %) and frequency (6 %) to have a comparatively restricted distribution, is more important than P. gardineri (Foslie) Foslie (2 % cover). P. onkodes maintains and provides the surf-resistant reef edge and is, therefore, of great ecological importance. Coelenterate corals cover less than 1 % of the total area and are relatively unimportant on the fringing reef. The hypothesis is developed that the high ratio (200 : 1) of crustose corallines to corals at Waikiki may be partly due to increases in eutrophication.Experimental evidence shows that P. onkodes can withstand intense illumination and is thereby unique among Hawaiian crustose Corallinaceae. Sporolithon erythraeum is more typical of other crustose corallines since it is physiologically adapted to low-light habitats.     

Sleep and blood pressure.

Direct arterial pressure was recorded continuously over 24 hours in 18 totally unrestricted people (six normotensives, four untreated hypertensives, and eight treated hypertensives). There was an almost equal fall of about 20% in both systolic and diastolic blood pressure during sleep in the three groups when compared with their waking pressures. This fall in pressure was greater than that observed previously in patients sleeping in a laboratory or hospital. Furthermore, it suggests that hypertensive subjects do not have a higher centrally-induced vasoactive component and that hypotensive drugs do not alter the pattern of blood pressure behaviour induced by sleep.     

Divergent contractile and structural responses of the murine PKC-epsilon null pulmonary circulation to chronic hypoxia

Loss of PKC-epsilon limits the magnitude of acute hypoxic pulmonary vasoconstriction (HPV) in the mouse. Therefore, we hypothesized that loss of PKC-epsilon would decrease the contractile and/or structural response of the murine pulmonary circulation to chronic hypoxia (Hx). However, the pattern of lung vascular responses to chronic Hx may or may not be predicted by the acute HPV response. Adult PKC-epsilon wild-type (PKC-epsilon(+/+)), heterozygous null, and homozygous null (PKC-epsilon(-/-)) mice were exposed to normoxia or Hx for 5 wk. PKC-epsilon(-/-) mice actually had a greater increase in right ventricular (RV) systolic pressure, RV mass, and hematocrit in response to chronic Hx than PKC-epsilon(+/+) mice. In contrast to the augmented PA pressure and RV hypertrophy, pulmonary vascular remodeling was increased less than expected (i.e., equal to PKC-epsilon(+/+) mice) in both the proximal and distal PKC-epsilon(-/-) pulmonary vasculature. The contribution of increased vascular tone to this pulmonary hypertension (PHTN) was assessed by measuring the acute vasodilator response to nitric oxide (NO). Acute inhalation of NO reversed the increased PA pressure in hypoxic PKC-epsilon(-/-) mice, implying that the exaggerated PHTN may be due to a relative deficiency in nitric oxide synthase (NOS). Despite the higher PA pressure, chronic Hx stimulated less of an increase in lung endothelial (e) and inducible (i) NOS expression in PKC-epsilon(-/-) than PKC-epsilon(+/+) mice. In contrast, expression of nNOS in PKC-epsilon(+/+) mice decreased in response to chronic Hx, while lung levels in PKC-epsilon(-/-) mice remained unchanged. In summary, loss of PKC-epsilon results in increased vascular tone, but not pulmonary vascular remodeling in response to chronic Hx. Blunting of Hx-induced eNOS and iNOS expression may contribute to the increased vascular tone. PKC-epsilon appears to be an important signaling intermediate in the hypoxic regulation of each NOS isoform.