Between discrete and continuous: consumer-resource dynamics with synchronized reproduction.

In many consumer-resource systems the consumer population has synchronized reproduction at regular intervals (e.g., years) but consumes the resource and dies continuously, while the resource population grows continuously or has overlapping generations that are short relative to the time between consumer reproductive events. Such systems require "semi-discrete" models that have both discrete and continuous components. This paper defines and analyzes a canonical, semi-discrete model for a widespread class of consumer-resource interactions in which the consumer is a discrete breeder and the resource reproduction can be described continuously. The model is the analog of the Nicholson-Bailey and Lotka-Volterra models for discrete and continuous systems, respectively. It thereby develops the basis for understanding more realistic, and hence more complex, semi-discrete models. The model can display stable equilibria, consumer-resource cycles, and single-species-like overcompensation cycles. Cycles are induced by high maximum fecundity in the consumer. If the resource grows rapidly and the consumer has high maximum fecundity, the model reduces to a single-species discrete-time model of the consumer, which can exhibit overcompensation cycles. By contrast, such cycles in discrete consumer-resource models typically occur only in the resource once the consumer is extinct. Also unlike a common class of discrete models that do not display consumer-resource cycles with periods below four years, semi-discrete models can exhibit consumer-resource cycles with periods as short as two years.

Single-species models for many-species food webs.

Most species live in species-rich food webs; yet, for a century, most mathematical models for population dynamics have included only one or two species. We ask whether such models are relevant to the real world. Two-species population models of an interacting consumer and resource collapse to one-species dynamics when recruitment to the resource population is unrelated to resource abundance, thereby weakening the coupling between consumer and resource. We predict that, in nature, generalist consumers that feed on many species should similarly show one-species dynamics. We test this prediction using cyclic populations, in which it is easier to infer underlying mechanisms, and which are widespread in nature. Here we show that one-species cycles can be distinguished from consumer resource cycles by their periods. We then analyse a large number of time series from cyclic populations in nature and show that almost all cycling, generalist consumers examined have periods that are consistent with one-species dynamics. Thus generalist consumers indeed behave as if they were one-species populations, and a one-species model is a valid representation for generalist population dynamics in many-species food webs.

Habitat structure and population persistence in an experimental community.

Understanding spatial population dynamics is fundamental for many questions in ecology and conservation. Many theoretical mechanisms have been proposed whereby spatial structure can promote population persistence, in particular for exploiter-victim systems (host-parasite/pathogen, predator-prey) whose interactions are inherently oscillatory and therefore prone to extinction of local populations. Experiments have confirmed that spatial structure can extend persistence, but it has rarely been possible to identify the specific mechanisms involved. Here we use a model-based approach to identify the effects of spatial population processes in experimental systems of bean plants (Phaseolus lunatus), herbivorous mites (Tetranychus urticae) and predatory mites (Phytoseiulus persimilis). On isolated plants, and in a spatially undivided experimental system of 90 plants, prey and predator populations collapsed; however, introducing habitat structure allowed long-term persistence. Using mechanistic models, we determine that spatial population structure did not contribute to persistence, and spatially explicit models are not needed. Rather, habitat structure reduced the success of predators at locating prey outbreaks, allowing between-plant asynchrony of local population cycles due to random colonization events.

Hypoxic exposure time dependently modulates endothelin-induced contraction of pulmonary artery smooth muscle.

Endothelins (ETs) have been implicated in the pathogenesis of hypoxia-induced pulmonary hypertension. We determined whether hypoxic exposure of rats (10% O2-90% N2, 1 atm, 1-48 days) altered contraction to ET in isolated segments of endothelium-denuded extralobar branch pulmonary artery (PA) and aorta. Hypoxic exposure increased hematocrit, right ventricular hypertrophy, and ET-1 plasma concentration. Hypoxia also caused a sustained decrease in PA but not in aorta sensitivity to ET-1. In comparison, hypoxic exposure throughout 12 days decreased time dependently the maximum contraction of PA to ET-1, BaCl2, and KCl. The hypoxia-induced decrease in maximum contraction of PA to ET-1 returned toward normal levels by 21 days and approximated control levels by 48 days. After 14 days of hypoxia, right ventricular hypertrophy correlated with decreased sensitivity of PA to ET-1. After 21 days of hypoxia, PA sensitivity to ET-2 and ET-3 was decreased, and sarafotoxin S6c-induced contraction was abolished. In conclusion, hypoxic exposure time dependently modulates the responsiveness of PA smooth muscle to ETs, BaCl2, and KCl. The hypoxia-induced changes in tissue responsiveness to ET-1 may be associated with increased plasma concentrations of this peptide.

Chronic hypoxia increases staurosporine sensitivity of pulmonary artery smooth muscle to endothelin-1.

Endothelins (ET) have been implicated in the pathogenesis of hypoxia-induced pulmonary hypertension. We evaluated the contribution of protein kinase C (PKC) to the ET-1 response of isolated endothelium-denuded extralobar pulmonary artery (PA) from rats exposed to chronic hypoxia (10% O2-90% N2, 1 ATM, 14 days or 28 days) or air. Hypoxia increased hematocrit (Hct [% above air control]: at 14 days, by 28+/-2%; after 28 days to 33+/-2%) and the mass ratio of right ventricle over left ventricle plus septum (RV/LV+S [% above air control]: at 14 days, by 54+/-1%; after 28 days to 114+/-13%), an index of right ventricle hypertrophy. Hypoxic exposure for 14 days and 28 days decreased PA sensitivity to ET-1 (change in EC50: 14 days, four-fold; 28 days, two-fold vs. air controls) and transiently decreased the magnitude of maximum ET-1-induced contraction (Emax [% decrease from control]: 14 days, 53+/-6%; 28 days, 23+/-6%). Staurosporine, a PKC inhibitor, decreased ET-1 sensitivity of PA from 0, 14, and 28 days air-exposed rats by four- to nine-fold without affecting Emax. However, staurosporine markedly decreased hypoxic PA sensitivity to ET-1 (change in EC50: 14 days, 1700-fold; 28 days, 55-fold vs. hypoxic controls) and decreased Emax (% decrease from hypoxic control: 14 days, 38+/-6%; 28 days, 59+/-7%). In conclusion, hypoxic exposure time-dependently varies the responsiveness of PA smooth muscle to ET-1 and may modulate the contribution of PKC activation.

Functional comparison of endothelin receptors in human and rat pulmonary artery smooth muscle.

The receptors mediating arterial smooth muscle contraction to endothelins (ET) differ among species and origin of vascular bed. We characterized ET receptors mediating contraction of endothelium-denuded human intralobar pulmonary artery (hIPA) and rat intralobar (rIPA) and extralobar left branch (rLPA) pulmonary artery with ET-1, ET-2, ET-3, sarafotoxin S6c, sarafotoxin S6b, and ET receptor antagonists in vitro. Rat aorta was studied for comparison. Each vascular segment showed concentration-dependent contraction with a rank order sensitivity (pD2) profile of ET-1 > or = ET-2 = sarafotoxin S6b > ET-3. Maximum contraction to ET-1 was greater than to sarafotoxin S6c in all preparations. Responses of rIPA and rLPA to sarafotoxin S6c were conspicuous when compared with hIPA or aorta. The ET(A) receptor blockers BQ-123 and BMS-182874 competitively antagonized ET-1 responses of hIPA and aorta, but not rLPA. The ET(B) receptor antagonist BQ-788 attenuated contractions of rIPA and rLPA to ET-3 and sarafotoxin S6c, respectively. In conclusion, ET(B)-mediated contraction of endothelium-denuded conduit pulmonary arteries varies among species and may contribute more to contraction of rIPA and rLPA than of hIPA and aorta, although maximum ET(B)-mediated contraction is smaller than that mediated by the ET(A) receptor.

Aggregation and stability in metapopulation models.

We analyze a metapopulation model of the interactions between Lotka-Volterra-type prey and predators that occur in two environmentally distinguishable patches and are linked by migration. Environmental differences between the patches tend to stabilize the otherwise neutrally stable model by causing the per capita immigration rate on a patch to be temporally density-dependent, partly as a consequence of out-of-phase fluctuations in density. However, the environmental differences can also lead to indirect effects on the temporal dependence of per capita prey death rate on prey density in each patch and on temporal dependence of per capita predator birthrate on predator density in each patch. Spatially density-dependent movement by the prey can be either uniformly destabilizing or initially stabilizing and then destabilizing as the degree of density dependence increases, depending on the overall rate of prey movement. Aggregation by the predator to the patch with more prey modifies one or more of the three processes listed above. Typically, weak aggregation is stabilizing, and strong aggregation is destabilizing. Aggregation can also render unstable an initially stable model. We conclude that metapopulation and single-population models are not good analogues of each other and that predator aggregation affects the two types of models via different mechanisms.